Neurology I Final Examination Review • Lesion B – clinically, patients complain of tunnel-like

COVERAGE vision, seen in cases of pituitary adenoma (pituitary tumor

I. Introduction to Clinical Neurosciences with size enough to impinge the optic chiasm)
II. Neuroanatomy • Lesion D – seen in cases of cerebrovascular disease
III. Neurologic History Taking and Examination involving M1 segment of the middle cerebral artery
IV. Neurolocalization (causing infarction of lateral geniculate nucleus)
V. Motor Weakness – Lower Motor Neuron System • Lesion E – loosely called “pie in the sky” and seen in
VI. Motor Weakness – Upper Motor Neuron System temporal lobe lesions (since the inferior optic radiations are
VII. Altered Sensorium and Syncope located in the temporal lobe)
VIII. Somatosensory Disorders
• Lesion F – seen in parietal lobe lesions (since the superior
IX. Dizziness and Dysequilibrium
optic radiations are located in the parietal lobe)
X. Epilepsy and Other Seizure Disorders
XI. Headache and Craniofacial Pain • Lesion G – similar to lesion D but there is characteristic
XII. Cerebrovascular Disease macular sparing (preservation of central vision) due to dual
Disclaimer and Note: These notes are compiled from different sources (lecturers, arterial supply of the macula from the middle cerebral
book, online peer-reviewed references) and are not intended to be used as the artery and posterior cerebral artery.
sole source for one’s review for the final examination. It must be used merely as
a guide as the student intends to reinforce previously learned knowledge and MOTOR PATHWAYS
integrate additional information from his/her reading in preparation for the
examination. May this review guide serve the student well as he/she intends to • In a patient presenting with motor dysfunction, tracing the
pass the subject with flying colors and appreciate the beauty of Neurology. anatomy of motor system from the upper motor neurons until
the lower motor neurons is critical. Remember the
INTRODUCTION TO CLINICAL NEUROSCIENCES Homunculus of Penfield since this a representation of the
• Diagnosis of neurological cases involve answering two key amount of innervation each body part receives in relation to
questions: (1) Where is the problem? (2) What is the its functional importance.
problem? (1) must always precede (2), not vice versa. • GENERALITIES:
• There are five pathways that the medical student must know: • (1) Corticobulbar = Corticonuclear. This tract supplies the
• (1) Visual Pathway head and neck, with the exception of the VAGUS NERVE
• (2) Motor Pathways: Corticospinal and Corticobulbar Tracts that supplies also the thoracic and abdominal areas.
• (3) Sensory Pathways: Dorsal Column – Medial Lemniscal • (2) Corticospinal tract supplies everything below the head
System (DCML) and Anterolateral/Spinothalamic Tract and neck.
(ALS/STT) • (3) Both the corticospinal and corticobulbar tracts CROSS
VISUAL (OPTIC) PATHWAY to the opposite side, only at different levels. All lesions
above the decussation cause CONTRALATERAL lesions.
• In a patient presenting with blurring of vision, thorough
All lesions below the decuessation cause IPSILATERAL
knowledge of the anatomy of the visual pathway guides the
lesions.
medical student in localizing lesions due to the unique
architecture of the visual pathway. • (4) The boundary between the upper and lower motor
neuron is the ANTERIOR HORN CELL.
• GENERALITIES:
• (1) TEMPORAL fibers of the optic nerve DO NOT CROSS
but NASAL fibers of the optic nerve CROSS to other
opposite side.
• (2) Optic NERVE -> Optic CHIASM -> Optic TRACT ->
LATERAL GENICULATE Nucleus -> Optic RADIATION ->
OCCIPITAL CORTEX. Do not interchange tract and
radiation.

Figure 2. Corticospinal and Corticobular Tracts

• Familiarize Figure 2 very well. Tracing the motor pathways
Figure 1. Visual Pathway and Corresponding Lesions
• Familiarize Figure 1 very well. Additional explanation include
the following:
• Lesion A – also called monocular blindness, seen in
cases of optic neuritis (inflammation of the optic nerve in
diseases such as Neuromyelitis Optica and Multiple
Sclerosis)
starts from the motor cortex to the corresponding muscles of
the head, neck, trunk, and upper and lower extremities. The
following is the pathway of the corticospinal tract:
• (1) Precentral gyrus = Primary Motor Cortex
• (2) Corona radiata – white matter projections
• (3) Internal capsule
• (4) Midbrain – specifically the cerebral peduncles
• (5) Pons – specifically the basis pontis
• (6) Medulla – specifically the pyramids (decussation
occurs at this level, 85% becomes the lateral corticospinal
tract whereas the remaining 15% that do not decussate
becomes the anterior corticospinal tract)
 • (7) Anterior horn cell – boundary between upper motor
neuron and lower motor neuron system
• (8) Projections to the upper and lower extremities
• Terminologies: -paresis (= weakness), -plegia (= paralysis)
• In a patient manifesting with weakness or paralysis of
specific parts of the body, there are certain generalities to
help the medical student localize lesions.
• (1) Right or Left Lower Extremity Weakness – lesion is at
the level of the spinal cord
• (2) Bilateral Lower Extremity Weakness – lesion is at the
level of the thoracic spinal cord
• (3) Bilateral Upper and Lower Extremity Weakness – lesion
is at the level of cervical spinal cord
• (4) Contralateral upper and lower extremity weakness with
Ipsilateral facial lesion – lesion at the level of the
brainstem (so called “crossed symptoms”)
• (5) Weakness on one side of the body – lesion is at the
level of the supratentorium (if with aphasia – probably
cortical lesion, if without aphasia – probably subcortical
lesion)
• Differentiation between upper and lower motor neuron
lesions is paramount and involves a thorough motor
examination during the neurologic examination. Remember
that these are GENERALITIES and there are always some
exceptions.
UMN Lesion LMN Lesion
Reflex Hyperreflexia Hypo/Areflexia
Tone Hypertonic/Spasticity Hypotonic/Flaccid
Babinski (+) (-)
Atrophy (-) (+)
Fasciculation (-) (+)
• Reflex and tone – the reason for an increase in these
components in UMN lesions is due to the loss of
modulation from the corticofugal fibers from the cortex.
Think of the UMN as your typical strict parents such that
when they are out of town (“UMN lesion”), chaos results
(“hyperreflexia and hypertonia”)
• Babinski reflex – this is a pathologic reflex that manifests
due to loss of inhibition of primitive reflexes by the frontal
lobe. In a neonate, infants and children up to 2 years of
age, Babinski sign is normally seen. Beyond 2 years of age
and in adults, the presence of this reflex indicates an UMN
lesion. Classically, this is seen in stroke, ALS and multiple
sclerosis, which all involve UMN lesions. On neurologic
examination, this is elicited by rubbing a blunt instrument
along the lateral side of the sole of foot from the heel then
making a curve along the toes.
• Atrophy and fasciculation – the reason for these two
phenomena in LMN lesions is due to loss of direct neural
stimulation of the muscles. Remember the muscles depend
on the neuromuscular junction not just for its function but
because the neural stimulation maintains these muscles.
Fasciculations are involuntary contractions or muscle
twitches resulting from loss of voluntary control from the
LMN over its corresponding projections.
SENSORY PATHWAYS
• In a patient presenting with sensory dysfunction, tracing the
anatomy of sensory system from the peripheral sensory
receptors until the sensory cortex is paramount. Remember
the Homunculus of Penfield since it represents the amount of
innervation a body part receives in relation to its functional
importance.
• GENERALITIES:
• (1) Anterolateral System is responsible for transmission of
pain, temperature and crude touch. Upon entry into the
spinal cord, it IMMEDIATELY DECUSSATES to the
opposite side.
• (2) Dorsal Column Medial Lemniscal System is responsible
for transmission of fine touch, pressure, vibration and
proprioception. Upon entry into the spinal cord, it ascends
IPSILATERALLY then DECUSSATES AT THE LEVEL OF
MEDULLA to the opposite side.
• (3) First-order neurons generally start from the peripheral
sensory receptors until the spinal cord. Second-order
neurons start from the spinal cord until the thalamus. Third-
order neurons start from the thalamus until the
somatosensory cortex.
Figure 3. Anterolateral and Dorsal Column Medial Lemniscal
Pathways
• Familiarize Figure 2 very well. Tracing the motor pathways
starts from the motor cortex to the corresponding muscles of
the head, neck, trunk, and upper and lower extremities. The
following is the pathway of the corticospinal tract:
• (1) Peripheral sensory receptors
• (2) Dorsal root ganglion
• (3) Spinal cord – anterolateral system decussates while
dorsal column medial lemniscal system ascends
ipsillaterally
• (4) Brainstem – anterolateral continuously ascends
ipsilaterally while dorsal column medial lemniscal system
decussates at the level of the medulla
• (5) Thalamus – different thalamic nuclei receive the
sensory fibers
• (6) Postcentral gyrus = Primary Somatosensory Cortex
• Terminologies: -esthesia (sensation), -algesia (pain)
NEUROANATOMY
• Review of neuroanatomy will include the following:
• (1) Cerebral Cortex
• (2) Cranial Nerves
• (3) Motor System
• (4) Sensory System
• (5) Reflexes
• (6) Cerebellum
• (7) Extrapyramidal Tracts and Basal Ganglia
• (8) Cerebrovascular System
CEREBRAL CORTEX
• Mainly responsible for awareness and requires an intact
ARAS (located in the middle to upper pons) for wakefulness.
• Divided into functional areas with correspondingly labeled
Brodmann’s Area, the most important of which are the ff:
 • Primary Somatosensory Cortex – BA 1,2,3
• Primary Motor Cortex – BA 4 (“4 limbs”)
• Sensory Association Cortex – BA 5,7
• Pre-motor Area – BA 6
• Frontal Eye Field – BA 8 (“8 ~ ∞”)
• Primary Visual Cortex – BA 17 (“1+7 = 8 ~ ∞”)
• Secondary Visual Cortex – BA 18,19
• Primary Auditory Cortex – BA 41
• Auditory Association Cortex – BA 42
• Wernicke’s Area – BA 22
• Broca’s Area – BA 44,45
• 10% - Primary Areas, 80-90% - Association Areas
• Primary Area – direct connection to and from receptors
• Secondary Area – makes sense of information from 1° areas
• Association Area – reception and analysis of information from
multiple cortical regions
• (1) Parieto-occipito-temporal – integrates information
from sensory, visual and auditory areas
• (2) Pre-frontal – plans complex patterns and movements
• (3) Limbic - integrates behavior, motivation and emotions
with sensory information (“Our brain tends to remember
memories that elicit human emotions”)
• Special Function Areas: Wernicke’s and Broca’s Areas
(usually in the left hemisphere)
• Wernicke’s – located in the superior temporal lobe,
functions as interpretative area of language, lesion in this
area results to RECEPTIVE aphasia (inability to interpret
written/spoken words)
• Broca’s – located in the left lateral frontal lobe, functions
for control of motor functions involved with speech, lesion in
this area results to EXPRESSIVE aphasia (inability to
produce speech)
• Note: GLOBAL aphasia results if both Wernicke’s and
Broca’s areas are damaged.
• There are 6 important lobes, and their functions are the ff:
• Frontal Lobe – conscious thought-reasoning-planning,
speech-movement, emotions-executive function, inhibition
of primitive reflexes, problem solving
• Parietal Lobe – perception-recognition-integration of
sensory stimuli
• Occipital Lobe – visual function and processing
• Temporal Lobe – smell, taste, sound perception-
recognition and integration, memory storage
• Insular Lobe (“Island of Reil”) – gustation
• Limbic Lobe – emotions, memory formation and learning
LESIONS OF THE CEREBRAL CORTEX
• Terminologies that are important to master are the ff:
• -paresis: weakness, -plegia: paralysis,
• Palsy: uncontrollable tremors
• Apraxia: inability to carry out motor activities on command
• Aphasia: inability to comprehend spoken/written words
• Ataxia: inability to coordinate voluntary movements
• Agnosia: inability to recognize familiar objects
• Prosopagnosia: inability to recognize faces
• Anosognosia: denial of neurologic deficit
• Dysnomia: impairment in recalling words/names
• Anosmia: inability to perceive odors
• -anopsia: blindness in a visual field
• Achromatopsia: decreased light sensitivity, vision and color
blindness
• Alexia: inability to understand written words
• Dyslexia: impairment in reading and comprehension
• Dysmetria: under/overshoot of targeted movements
• Dysdiachokinesia: inability to perform rapid alternating
movements
• Abulia: lack of willpower/initiative
• Akinetic mutism: tending not to move/speak
• Saccades: fast eye movements
• Nystagmus – involuntary, rapid and repetitive
movements of the eyes
• FRONTAL LOBE lesions involve affectation of the (1) motor
area, (2) prefrontal cortex, (3) olfactory nerve, (4) Broca’s
area, (5) parasagittal frontal lobe. Symptoms arise from
damage to these structures, such as the ff:
UNILATERAL FRONTAL LOBE DISEASE: R or L
(1) Contralateral spastic hemiplegia and hemiparesis – due to
affectation of motor area
(2) Symptoms of disinhibition (elevation of mood, increased
talkativeness, tendency to joke inappropriately), lack of tact,
difficulty in adaptation and loss of initiative – due to affectation
of prefrontal area
(3) Frontal release signs (grasp and suck reflexes) – due to
affectation of the prefrontal area
(4) Anosmia – due to affectation of olfactory tract in the area
of the orbitofrontal lobe
*If entirely prefrontal area damage: no hemiplegia
LEFT FRONTAL LOBE DISEASE
(1) Right-sided spastic hemiplegia and hemiparesis
(2) Broca’s aphasia, +/- apraxia of the lips and tongue – due to
affectation of left lateral frontal lobe and motor area
innervating the lips and tongue (remember the Homunculus
of Penfield from which the lips and tongue have the greatest
motor innervation)
(3) Sympathetic apraxia of the left hand – due to affectation of
the dominant frontal lobe causing decreased transmission
from the command center (the dominant frontal lobe) to the
right frontal lobe (which controls the left hand)
*Same as (2), (3), (4) from above
RIGHT FRONTAL LOBE DISEASE
(1) Left-sided spastic hemiplegia and hemiparesis
*Same as (2), (3), (4) from above
BILATERAL FRONTAL LOBE DISEASE
(1) Bilateral hemiparesis – due to affectation of bilateral motor
areas
(2) Pseudobulbar palsy – paralysis, weakness and
hyperreflexia of the muscles in the face, mouth and pharyngeal
area due to affectation of the corticobulbar tract from the
motor area (vs. bulbar palsy wherein there is direct affectation
of the cranial nerve nuclei. You can think of this as the
equivalent of LMN lesion in the spinal cord where anterior horn
cell = cranial nerve nuclei)
(3) Abulia, akinetic mutism, inability to sustain attention and
solve problems, rigid thinking, bland affect, behavioral
disinhibition, labile mood, frontal release signs, utilization
behavior – due to affectation of the prefrontal area
(4) Gait decomposition and sphincter incontinence – due to
affectation of the parasagittal frontal lobe, which controls the
lower extremities.
• PARIETAL LOBE lesions involve affectation of the (1)
sensory cortex, (2) sensory association areas, and (3)
superior loop of the optic radiation. This is where you will
observe unusual sensory symptoms and deficits. Symptoms
arise from damage of these structures, such as the ff:
UNILATERAL PARIETAL LOBE DISEASE: R or L
(1) Corticosensory syndrome and contralateral sensory
extinction – causes deficits in identifying more complex
sensations such as direction, 2-point discrimination and
shape that require sensory cortical integration whereas pain,
temperature and touch are usually spared since this integration
is already sufficient at the level of the thalamus
(2) Mild hemiparesis, hypotonia, poverty of movement and
hemiataxia – due to affectation of the corticospinal tract (a
portion of which originates from the parietal lobe)
(3) Inferior quadrantanopia – due to affectation of the superior
loop of the optic radiations that pass through the parietal
lobe (superior loop responsible for the inferior visual field)
(4) Abolition of optokinetic nystagmus with target moving
towards contralateral side of the lesion – due to affectation of
the contralateral parietal lobe (normally, repeated movement
of the object and repeated detection will manifest as
nystagmus and this is a physiologic response such as when
you are in a moving train looking outside at a stationary object;
with affectation of the parietal lobe, once an object moves
towards the side opposite the affected parietal lobe, the object
disappears and is no longer recognized by the brain and the
normal optokinetic nystagmus can no longer be seen).
(5) Contralateral hemineglect – due to affectation of the
parietal lobe (patients will tend to only recognize one side of
the body with gaze preference towards the only side that is
recognizable)
LEFT PARIETAL LOBE DISEASE
(1) Alexia – due to affectation of the angular gyrus that is
located in the dominant parietal lobe, responsible for reading
and writing
(2) Gerstmann Syndrome – manifests as a tetrad of symptoms
including Right-left disorientation (inability to discriminate left
and right sides of the body), finger agnosia (inability to
recognize one’s own fingers or the examiner’s fingers),
a/dyscalculia (impaired calculation), a/dysgraphia (impaired
writing), due to affectation of the dominant parietal lobe
(3) Tactile agnosia – inability to recognize objects placed in the
hand (You can give the patient a familiar object such as a coin
and they will not recognize it)
(4) Bilateral ideational and ideomotor apraxia – ideational (=
failure in conceptualization) apraxia is the inability to carry out
functions that rely on semantic memory (eg. skill memory such
as brushing teeth and combing hair) while ideomotor (=
breakdown in concept and performance) apraxia is the
inability to imitate actions but spontaneous actions remain
intact (eg. asking and demonstrating to a patient on how to
comb one’s hair but he/she cannot do it on command but
without your command, the patient performs the task)
RIGHT PARIETAL LOBE DISEASE
(1) Predominantly hemineglect
(2) Visuospatial disorders – inability to perceive the
relationship of objects in space to one another or to oneself
(3) Topographic memory loss – inability to go from one place
to another, +/- map
(4) Anosognosia, dressing and constructional apraxia – denial
or unawareness of neurologic deficit and difficulties in
performing complex tasks such as dressing, building,
assembling and drawing objects, respectively.
(5) Confusion, eyelid apraxia – tendency to keep eyes closed,
resist lid opening and blepharospasm
BILATERAL PARIETAL LOBE DISEASE
(1) Visual spatial imperceptions, spatial disorientation,
(2) Complete or Partial Balint’s Syndrome – the syndrome is
secondary to affectation of the parietotemporal and parieto-
occipital areas, it is characterized by (1) spatial
disorientation, (2) hemineglect, (3) optic apraxia (inability to
move eyes on command but can spontaneously move eyes)
and (4) simultagnosia (inability to perceive more than one
object at a time, resulting in inability to perceive things as a
whole)
• TEMPORAL LOBE lesions involve affectation of the (1)
auditory cortex, (2) auditory association areas, (3) Wernicke’s
area, (4) hippocampal formation, (5) amygdala and (6)
inferior loop of the optic radiation. Symptoms arise from
damage of these structures, such as the ff:
UNILATERAL TEMPORAL LOBE DISEASE: R or L
(1) Auditory, visual, olfactory and gustatory hallucinations
(2) Dreamy state – due to affectation of the uncus seen in
uncinate seizures
(3) Delirium and Disturbances in time perception
LEFT TEMPORAL LOBE DISEASE
(1) Homonymous contralateral upper quadrantanopsia – due to
affectation of the inferior loop of the optic radiations
(2) Wernicke’s Aphasia – due to affectation of left superior
temporal lobe
(3) Amusia – impairment in interpretation of music
(4) Impairment in tests of verbal material presented via the
auditory sense
(5) Dysnomia or amnesic aphasia – difficulty in recalling
names/words, probably due to affectation of hippocampus
(6) Visual agnosia – inability to recognize visually-presented
objects (As you can observe, there are some exceptions and
not all that is visual in deficit is purely occipital)
(7) Korsakoff Syndrome – difficulty recalling and confabulates
memories (confabulation as a compensation to make up for
lost memory), probably due to affectation of hippocampus
RIGHT TEMPORAL LOBE DISEASE
(1) Homonymous contralateral upper quadrantanopsia
(2) Impairment in tests of visually-presented nonverbal material
(3) Agnosia for sounds and some qualities of music
(4) Occasional inability to judge spatial relationships (Again,
another exception where spatial is not purely parietal)
BILATERAL TEMPORAL LOBE DISEASE
(1) Korsakoff amnesic defect – due to affectation of
hippocampus
(2) Hypermetamorphosia – compulsion to attend to all visual
stimuli
(3) Apathy and Placidity
(4) Kluver-Bucy Syndrome – due to affectation of the
amygdala and is characterized by fearless attitude and
extreme curiosity about anything, rapid forgetfulness, places
everything in the mouth and hypersexuality
• OCCIPITAL LOBE lesions involve affectation of the (1) visual
cortices, and (2) visual association areas. Symptoms arise
from damage of these structures, such as the ff:
UNILATERAL OCCIPITAL LOBE DISEASE: R or L
(1) Contralateral homonymous hemianopsia – with (peripheral)
or without (central) macular sparing; if (+) macular sparing it is
usually seen in PCA stroke due to dual blood supply of the
macula from the PCA and MCA; if (-) macular sparing it is
usually seen if the lesion at the level of ICA
(2) Homonymous hemiachromatopsia
(3) Elementary (unformed) hallucinations – due to irritative
lesions of the occipital cortex, more complex hallucinations are
due to damage of the occipitoparietal and occipitotemporal
lobes
LEFT OCCIPITAL LOBE DISEASE
(1) Right-sided homonymous hemianopsia
(2) Visual agnosia – due to affectation of the association
areas (Remember that association areas serve highly
specialized functions. Recognizing an object visually requires
not only vision but integration with its sensory meaning)
(3) Alexia and color-naming defect – due to affectation of deep
white matter or splenium of the corpus callosum
(Remember that the corpus callosum is involved in connecting
the two cerebral hemispheres allowing the command center
from the dominant hemisphere to control the non-dominant
hemisphere)
RIGHT OCCIPITAL LOBE DISEASE
(1) Left-sided homonymous hemianopsia
(2) Topographic memory loss and loss of visual orientation –
remember that in right-sided parietal lobe lesions, these
symptoms also emerge and this is probably due to affectation
of the right occipitoparietal area
(3) Visual illusions (metamorphosia) and hallucinations – due
to extensive occipital lobe lesions with hallucinations more
common in the R > L occipital lobe
BILATERAL OCCIPITAL LOBE DISEASE
(1) Cortical blindness but intact pupillary reflex – due to
sparing of the oculomotor nucleus since its nucleus is
located in the midbrain (Edinger-Westphal Nucleus)
(2) Anton Syndrome (visual anosognosia) – denial of blindness
(3) Achromatopsia – loss of color perception
(4) Prosopagnosia – loss facial recognition due to affectation
of the occipitotemporal area, specifically the fusiform gyrus
(5) Simultagnosia – due to affectation of occipitoparietal area
(6) Balint’s Syndrome – due to affectation of bilateral dorsal
high occipitoparietal area
*Visual hallucinations with added objections/information usually
involves temporal lobe disease while visual distortions usually
involve occipital lobe disease
• Limbic system – responsible for emotions, an important part
of memory formation and learning. It is composed of the ff:
• (1) Orbitofrontal gyrus – area above the olfactory tract
• (2) Cingulate gyrus – area above the corpus callosum
• (3) Subcallosal gyrus – aka Zuckerkandl’s gyrus
• (4) Parahippocampal gyrus – area surrounding the
hippocampal formation
• Other parts: hippocampus (compared to the cerebral
cortex, contains only 3 histological layers), dentate gyrus,
supracallosal gyrus
CRANIAL NERVES
• CNs are can have sensory, motor or mixed functions. A
mnemonic to remember is Some Say Money Matters But My
Brother Says Big Brains Matter Most (from I – XII, S –
sensory, M – motor and B – both)
• Except for CN I and II, all the rest of the cranial nerves are
located in the brainstem.
• At the level of the MIDBRAIN lies CN III and IV
• Tectum – roof, Tegmentum – body, Cerebral peduncles
– where the corticospinal tract passes through
• At the level of the superior colliculus (responsible for vision)
lies the oculomotor nuclei and mesencephalic nucleus
of CN V
• At the level of the inferior colliculus (responsible for
hearing) lies the trochlear nucleus. Note that CN IV is the
only CN that decussates and exits dorsally in middle of the
superior and inferior colliculus in the dorsum of the
midbrain to innervate the contralateral superior oblique
muscle (ie. CN IV from the right part of the midbrain
innervates the left superior oblique, and vice versa)
• At the level of the PONS lies CN V, VI and VII
• CN V has the ff nuclei: mesencephalic (jaw position),
primary sensory (pain and temperature sensation) and
spinal
• CN VII wins around CN VI nuclei forming the facial
colliculus
• At the level of the MEDULLA lies CN VIII, IX, X, XI and XII
• CN X has the ff nuclei: dorsal nucleus (salivary glands,
heart and diaphragm), tractus solitarius (taste sensation
formed by CN VII, IX and X) and ambiguus (innervation of
throat muscles, formed by CN IX and X)
MOTOR SYSTEM
• Previously discussed but in addition, more lateral parts of the
Homunculus of Penfield are represented by the upper body
structures while the more medial parts are represented by
the lower body structures
• Primary motor tracts aka pyramidal tract and decussation
occurs at the lower medulla (fibers for the UE are the first to
decussate followed by fibers for the LE; hence, lesion in the
middle of the lower medulla can cause crossed weakness
where there ipsilateral UE weakness since fibers for the UE
have already decussated and contralateral LE weakness
since fibers for the LE have not yet decussated)
• Note that the corticospinal tract is influenced by the basal
ganglia involves in fine tuning of movements, as well as the
cerebellum and inhibitory interneurons involved in
coordination of movements.
• Remember the generalities and differentiation between UMN
and LMN. An additional pathologic reflex (aside from
Babinski reflex) that we can observe in UMN lesions
especially at the level of the cervical spine is the Hoffman
reflex. Lesions at lower spinal cord levels usually manifest
with only Babinski reflex.
SENSORY SYSTEM
• Dermatomes are not innervated by a single spinal nerve
(considerable overlap exists)
• DCML is responsible for position and vibration sense, 2-
point discrimination, fine touch, pressure
• Terminates at the VPL nuclei of the thalamus. The VPL
nucleus is usually the main sensory thalamic nuclei, except
for VPM nuclei where taste and nerve fibers from the
trigeminal nucleus terminate
• (From peripheral to central): Sensory receptors -> Dorsal
root ganglion -> Nucleus Gracilis for LE (GRACE-ful LEGS)
and Nucleus Cuneatus for UE (C-unning HANDS) ->
Decussation at the level of medical lemniscus at upper
medulla -> pons (now called the internal arcuate fibers) ->
pons -> midbrain -> VPL nuclei -> Parietal Lobe
st
• 1 -order neurons: sensory receptors to DRG
nd
• 2 -order neurons: DRG to VPL thalamic nucleus
rd
• 3 -order nuclei: VPL thalamic nucleus to cerebral cortex
• ALS/STT is responsible for crude touch, pain, temperature
• Anterior: for light touch and pressure, decussation at 2-3
levels above the first-order neuron
• Lateral: for pain and temperature, decussation at same
level of the spinal cord
• (From peripheral to central): Sensory receptors -> Dorsal
root ganglion -> Decussation at the substantia gelatinosa
of spinal cord-> medulla (now called the spinothalamic
fibers) -> pons -> midbrain -> VPL nuclei -> Parietal Lobe
• Lesions of the Sensory System:
• Hypoesthesia, Anesthesia
• Paresthesia – spontaneous unpleasant, abnormal
sensations which are electrical in quality
• Dysesthesia – same as paresthesia but provoked
• Allodynia – non-noxious stimuli but perceived as painful (A
for Arte)
• Hyperpathia – noxious stimuli but exaggeratedly perceived
as painful
CEREBELLUM
• 3 anatomical lobes exist, namely the anterior, posterior and
flocculonodular lobes
• Anterior lobe – superior surface, separated from posterior
lobe by primary fissure
• Posterior lobe – largest part
• Flocculonodular lobe – separates superior and inferior parts
of the cerebellum, separated from posterior lobe by
posterolateral fissure
• 4 Nuclei (from medial to lateral) – Dentate, Emboliform,
Globose, Fastigial
• Motor homunculus exists
• Vermis – coordination of axial body movements
• 3 function subdivisions:
• Archicerebellum (VESTIBULOcerebellum) –
flocculonodular lobe and fastigial nuclei, functions for eye
orientation during movement and coordination of head and
limb position in different positions and while in motion,
 lesion in this subdivision causes nystagmus due to lack of
eye orientation, constant head nodding due to lack of
head coordination with the body
• Paleocerebellum (SPINOcerebellum) – anterior lobe and
globose and emboliform nuclei, functions for maintenance
of postural tone, lesion causes truncal ataxia due to loss
of postural tone maintenance
• Neocerebellum (CEREBRO/PONTOcerebellum)
posterior lobe and dentate nuclei, functions for coordination
and control and correction of movement, lesion causes
incoordination
• Lesions:
• Nystagmus, action tremor, dysmetria, dysdiachokinesia,
ataxia, titubation (rhythmic tremor of head and trunk),
overshoot
• Mnemonics (from our batchmate): The AFP went to the PAN
pacific war. They provided service (SVC). They acquired
traumatic brain injury (TBI) and that’s the AND (End) of their
lives.
Lobe Phylogeny Functional Role Lesion
Anterior Paleo Spino Tone Ataxia (Gait)
Flocculonodular Archi Vestibulo Balance Nystagmus
Posterior Neo Cerebro Incoordination Dysmetria
EXTRAPYRAMIDAL TRACTS AND BASAL GANGLIA
• Function: modulation of movement, supports voluntary
activity, principally controls proximal muscles
• Caudate Nucleus + Putamen – Striatum (main receiver of
afferent signals)
• Putamen + Globus Pallidus – Lentiform Nucleus
• Direct pathway stimulates movement, Indirect pathway
inhibits movement
• D1 receptors – stimulates movement
• D2 receptors – inhibits movement
• Lesions:
• Altered muscle tone – rigidity/dystonia due to loss of
coordination between contraction and relaxation of muscles
• Adventitious movements – tremors, chorea, athetosis,
hemiballismus
• Others: Masked expression, Glabellar Reflex (Myerson
Sign) becomes evident, Gait Instability
NEUROLOGIC HISTORY TAKING AND EXAMINATION
• Unique features of neurologic history taking include (1)
handedness (remember that 95% of the population are right-
handed), (2) address/residency (functions as a test of
memory and regional differences of diseases)
• Timing in neurology is extremely critical (eg. stroke [acute
onset] versus tumors [chronic onset])
NEUROLOGIC HISTORY TAKING
• Common neurologic symptoms include (1) headache, (2)
dizziness, (3) weakness, (4) numbness, (5) loss of
consciousness/altered sensorium, (6) seizures, (7) tremors
• Neurologic disorders can be classified into two types of brain
injury: (1) focal (usually localizable), (2) diffuse (usually
enough to cause cognitive impairment)
• The etiology of neurologic diseases can be localized based
on (1) structural (anatomical lesion) and (2) metabolic (eg.
infections, electrolyte imbalance)
Figure 4. Etiologies based on types and timing of brain injury
NEUROLOGIC EXAMINATION
• Must be as systematic as possible: (1) Level of
consciousness*, (2) MMSE, (3) Cranial Nerves, (4) Sensory,
(5) Motor, (6) Reflexes, (7) Cerebellum, (8) Gait and Balance,
and other special examinations as indicated (Meningeal
signs, sweat pattern, Lasegue’s test, Tinel’s sign, Phalen’s
maneuver).
– • Note that each examination must aide in the localization of
lesions pointing to a disease that will explain the patient’s
clinical manifestations and phenomenology. This also
establishes the patient’s baseline neurologic status.
• Mini Mental Status Examination
• Assess hearing and comprehension of simple conversation.
Allow patients to use hearing or visual aids if needed.
• A score of 0 is given if the person does not respond after
THREE times.
• Orientation to time and place [10 pts] -> Registration [3 pts]
-> Attention and Calculation [3 pts, serial sevens or world
spelled backwards] -> Recall [3 pts] -> Naming [2 pts] ->
Repetition [1 pt] -> 3-stage command [3 pts] -> Reading [1
pt] -> Writing [1 pt] -> Copying [1 pt]
• Lesions of the higher cortical systems result in abnormal
MMSE results.
• Cranial Nerves
• I (Olfactory) – note that patient’s eyes must be closed while
wafting the bottle and irritating substances cannot be used
as these will stimulate CN V
• II (Optic) – note that this includes visual acuity, visual fields
by confrontation, pupillary reflex and fundoscopy.
• III (Oculomotor), IV (Trochlear) and VI (Abducens) – note
that while making a wide H, observe for nystagmus during
upward and lateral gaze; remember LRA-SOT.
• V (Trigeminal) – note that all subdivisions must be tested
(forehead for V1, cheeks for V2 and jaw for V3) for sensory
function (always compare both sides!), corneal/blink reflex
and jaw jerk reflex
• VII (Facial) – note that aside from facial movements, taste
is also tested
• VIII (Vestibulocochlear) – note that Weber is for
lateralization (can be placed on any bony prominence),
Rinne is for comparing air and bone conduction while
Schwabach is for comparing results with the examiner’s.
• IX (Glossopharyngeal) and X (Vagus) – note that examiner
must observe the palatal elevation (ie. by saying “ah”) and
the gag reflex (elevation of tongue and soft palate) and
pharyngeal constriction
• XI (Spinal Accessory) – note that examiner must allow
patient to shrug shoulders or turn the head to each side first
before pushing the shoulders down
• XII (Hypoglossal) – note that examiner can ask patient to
push tongue against the inside of each cheek to test for
strength.
• Sensory
• Always compare BOTH sides.
• For pain and temperature, usually testing either one of the
two is sufficient
• For vibration and proprioception, remember to place tuning
fork on the DIP and not the nailbed for vibration and
demonstrate the positions of up and down before asking
patient to identify the position for proprioception.
• Do not test on calloused skin since it is insensitive.
• Motor
• Includes BULK, TONE, and STRENGTH.
• BULK: compare both sides and check if uni/bilateral and if
proximal/distal
• TONE: spasticity (velocity-dependent) versus rigidity
(velocity-independent), hypotonia
 • STRENGTH: note that dominant side is slightly stronger Peripheral Nerve
and note/master muscle strength grading Step 3. Intersections
• Testing for muscle strength can start from distal to proximal - Combining the symptoms, their intersection or a location,
or vice versa, whichever is more convenient which can explain the appearance of all the symptoms is the
• Reflexes CORTEX.
• Note that patient must be completely RELAXED to elicit the - Therefore, lesion is most likely in the CORTEX.
deep tendon reflexes. Remember/master the grading of - Using the 3Ls, we have just levelized the lesion to the
reflexes. CORTICAL area, lateralized that the lesion is on the LEFT side
• Physiologic: Biceps (C5-C6), Triceps (C6-C7), (due to right-sided weakness, gaze deviation to the left), and
Brachioradialis (C5-C6), Patellar (L2-L4), Achilles (S1) likely localizing that the lesion is in the FRONTAL lobe area.
• Pathologic (seen in UMN lesions): Babinski and Babinski- - Therefore, we have a lesion in the LEFT FRONTAL
like reflexes, Ankle clonus, Glabellar tap, Rooting, Grasp, CORTEX. Due to the sudden nature of the symptoms and age
Palmomental, Tromner’s-Hoffman’s-Rossolimo’s of the patient, it is likely VASCULAR etiology.
• Cerebellum Answer: Ischemic Infarction of the Left Frontal Lobe secondary
• Requires integrated function of the motor system, sensory to Occlusion of the Superior Division of the MCA
system, vestibular system and cerebellar system to create
COORDINATION NEURAXIS LEVELS – NEUROLOGIC EXAMINATION
• Examinations include (1) Finger-to-nose test, (2) Heel-to- • Cortex – familiarize the anatomic lobes and their functions
shin test, (3) Rapid Alternating Movements, (4) Romberg’s • Brainstem – I and II not in the brainstem, III-IV in the
• Observe for dydiachokinesia, overshoot and nystagmus if midbrain, V-VII – pons, VIII-XII - medulla
one is suspecting cerebellar lesions. • Corticospinal tract – remember the generalities of
• Gait and Balance differentiating UMN and LMN injury
• Examinations include observation of fluidity of normal gait, • Note: most of the corticobulbar tracts are bilateral. Hence it
tandem gait, heel and toe walking. would take a severe lesion large enough to create complete
• Note that to distinguish vestibular and cerebellar lesions weakness of the innervations of the corticobulbar tract
presenting as balance problems, ask the patient to open • Central versus Peripheral Facial Palsy: due to contralateral
the eyes and if the balance problem lessens/disappears, innervation to the lower part of the face versus bilateral
then the problem is VESTIBULAR due to compensation of innervation to the upper part of the face. More commonly
the eyes but if the balance problem persists despite having observed is central facial palsy seen in stroke patients,
the eyes open, then the problem is CEREBELLAR hence why facial asymmetry is a warning sign of stroke.
• Special Examinations • CN XII is also preferentially contralaterally innervated.
• Meningeal signs: Brudzinski (B for “Batok”) and Kernig (K Table 1. Motor Loss Patterns
for “Kernig”) Site of Lesion Motor Loss
• Sweat pattern: for Horner’s syndrome Cortex, Corona Radiata Contralateral Hemiparesis
• Phalen’s Sign: for Carpal Tunnel Syndrome Internal Capsule Central Facial Palsy
Brainstem Contralateral Hemiparesis
NEUROLOCALIZATION Ipsilateral Cranial Nerve
• HISTORY/PE accurately localized most lesions while Deficits
damage to different divisions produce UNIQUE clinical Spinal Cord Quadri/Paraparesis
deficits. Cranial Nerve Sparing
• Main goal: to explain all S/Sx on the basis of ONE LESION. Anterior Horn Cell Localized/generalized
• 3Ls: LEVELIZE, LATERALIZE and LOCALIZE [WHERE?] -> weakness
Pathophysiology [HOW?] -> Pathology [WHAT? Answered by Nerve Root Loss follows root distribution
the neurologic history] Nerve Plexus Loss follows more than 1
• Steps: (1) List down all abnormal findings -> (2) nerve root distribution
Neuroanatomic Correlation -> (3) Intersections (may consider Polyneuropathy Hands-Arms, Feet-Legs
two or more lesions if no intersections) Mononeuropathy Single peripheral nerve
• Hard signs localizable while soft signs poorly localizable. NMJ Fatigable pattern
• Neurologic examination guides localization Muscle Proximal>Distal muscles
• MMSE – Cortex • Sensory – remember STT/ALS that decussates upon entry
• Cranial Nerve – Brainstem into the spinal cord while DCML that decussates at the upper
• Motor Exam and Reflexes – Corticospinal Tract medulla (higher level than the corticospinal tract)
• Gait and Coordination – Cerebellum • Central sensory nucleus of CN V extends from pons up to
the spinal cord, with lesion presenting as facial numbness
Example of Application of Steps in Neurolocalization
• CN V nuclei: Mesencephalic nucleus for proprioception,
A 70-year old patient comes in with sudden onset (3 hours
Main sensory nucleus for touch and pressure, and Spinal
prior) of slurring of speech, right-sided weakness (1/5 on the
nucleus for pain and temperature
arms and face, 3/5 on the lower limbs), gaze deviation to the
left, and right-sided facial drooping. Table 2. Sensory Loss Syndromes
Step 1. List down all abnormal findings Lesion Sensory Loss
- Slurring of speech, right-sided weakness, gaze deviation to Parietal Cortex Contralateral sensory loss
the left, right-sided facial drooping Thalamus Contralateral sensory loss
Step 2. Neuroanatomic Correlation Brainstem Ipsilateral facial sensory loss
- Slurring of speech: Cortex, Subcortex, Brainstem, Spinal Contateral limb sensory loss
Cord, Peripheral Nerves Cauda Equina Legs and Perineum
- Right-sided weakness (UE and face>LE): Cortex Nerve Root Dermatamol
- Gaze deviation to the left: Cortex, Subcortex, Brainstem All Peripheral Nerves Glove and stocking
- Right-sided facial drooping: Cortex, Subcortex, Brainstem, Single Peripheral Nerve Nerve distribution

Table 3. Sensory Loss Syndromes
Lesion Sensory Loss
Complete spinal cord injury All levels below the lesion
Hemisection/Brown Sequard Ipsilateral – motor, vibration
Syndrome and position sense
Contralateral – pain and
temperature
Central Cord Syndrome Loss of pain and temperature
in band over segments
occupied by the lesion
• Cerebellum: part of gait and coordination along with the
motor, sensory systems and cortex
• Anterior lobe – regulates muscle tone, coordination of
skilled voluntary movement – lesion causes gait ataxia
• Posterior lobe – for planning of voluntary movements –
lesion causes limb ataxia and hypotonia
• Flocculonodular lobe – maintains balance, control of eye
movements – lesion causes titubation of head-trunk,
drunken gait, truncal ataxia
• Visual System: lesions cause loss of vision in PREDICTABLE
patterns
• Gaze Deviation – pathways starts at BA 8 (Frontal Eye
Field) -> internal capsule (anterior limb) -> decussates at
midbrain-pontine junction -> innervates PPRF -> innervates
CN VI and thereby lateral rectus muscle -> decussates
again back to the side of FEF activation via MLF ->
innervates medial rectus subnucleus of CN III and thereby
medial rectus. Hence, right FEF allows gaze towards the
left and cortical lesions (above the decussation) cause
gaze deviation towards the ipsilateral side of the lesion
while brainstem lesions (below the decussation) cause
gaze deviation towards the contralateral side of the lesion
• Anisocoria – unequal pupillary sizes and must differentiate
physiologic versus pathologic causes. Common
pathologic causes include Horner’s Syndrome and Third
Nerve Palsy.
ABNORMAL NEUROLOGIC FINDINGS
• Analyze structures found in each level and relate these
structures to your neuroanatomy and neurophysiological
functions.
• Cortical Brain
• Classic presentation is abnormal higher cortical function
(absence of which likely rules out cortical lesion)
• Neurologic examination (when cortical brain has a lesion:
abnormal higher cortical function, motor and sensory
dysfunction, hyperreflexia and pathologic reflexes, the
rest (cranial nerves, cerebellar) are normal.
• Subcortical Brain
• Classic presentation is equal involvement of face/arm/leg
(weakness and numbness) with visual field deficits
(quadrantanopsia)
• Neurologic examination (when subcortical brain has a
lesion): cranial nerve deficit (visual field cuts), motor and
sensory dysfunction (equal involvement, Face=UE=LE),
hyperreflexia and pathologic reflexes. The rest (higher
cortical function and cerebellar) are normal.
• Brainstem
• Classic presentation is crossed deficits (ipsilateral cranial
nerve deficits and contralateral motor/sensory dysfunction)
• Neurologic examination (when brainstem has a lesion):
cranial nerve deficit (except for CN I and II; III-IV-VI:
Diplopia, V: Facial Numbness, VIII: Facial Drooping, IX-X-
XII: Dysarthria and Dysphagia, XI: Decreased neck and
shoulder strength), motor and sensory dysfuntion,
hyperreflexia, pathologic reflexes. The rest (higher
cortical function, cerebellar) are normal.
• Cerebellum
• Classic presentation is HANDST (hypotonia, assynergy of
antagonist muscles, nystagmus,
dysmetria/dysdiachokinesia/dysarthria, stance and gait
instability, tremor)
• Neurologic examination (when cerebellum has a lesion):
cerebellar deficits, motor dysfunction (intention > resting
tremor, axial instability). The rest (higher cortical function,
cranial nerves, sensory, reflexes, pathologic reflexes) are
normal.
• Spinal Cord
• Classic presentation is weakness of distal/extensors >
proximal/flexors since corticospinal tract mainly controls
the distal extensors with sensory dysfunction at the
specific spinal cord level, and bowel/bladder involvement
(retention first then incontinence)
• Neurologic examination (when spinal cord has a lesion):
motor dysfunction (extensors>flexors, usually below the
lesion), sensory dysfunction (usually below the lesion),
hyperreflexia, and pathologic reflexes. The rest (higher
cortical function, cranial nerves, cerebellar) are ormal.
• Root
• Classic presentation is pain (sharp, stabbing, hot,
radiating) with sensory/motor dysfunction at the
dermatomal/myotomal level since nerve roots contain a
mixture of sensory and motor nerve fibers
• Neurologic examination (when nerve root has a lesion):
motor/sensory dysfunction (usually asymmetric, severe if
more than 1 nerve root is transected, remember that
dermatomal and myotomal levels usually overlap),
hypo/areflexia, pathologic reflexes (Spurling’s, Dural
Tension sign)
• Peripheral Nerve
• Classic presentation is distal-predominant motor and
sensory dysfunction (asymmetric) with possible
autonomic involvement and trophic changes (eg. skin, hair
and nails).
• Neurologic examination (when peripheral nerve has a
lesion): distal motor/sensory dysfunction (atrophy,
fasciculations, hypotonia, dysesthesias, hyperpathia,
allodynia), hypo/areflexia with possible cranial nerve
deficits. The rest (higher cortical function, cerebellar,
pathologic reflexes) are normal.
• Neuromuscular Junction
• Classic presentation is fatigability, proximal-symmetric
weakness with preserved muscle bulk/tone and
sensory function
• Neurologic examination (when NMJ has a lesion): fatigable
cranial nerve functions (ie. ptosis, dysconjugate gaze,
slack jaw), motor dysfunction, normo/hypo/areflexia.
The rest (higher cortical function, cerebellar, sensory,
pathologic reflexes) are normal.
• Muscle
• Classic presentation is proximal-symmetric UE-LE
weakness with cramping, aching, atrophy but
preserved sensation.
• Neurologic examination (when muscle has a lesion):
cranial nerve deficits (ie. ptosis, slack jaw, dysphagia,
dysarthria), motor dysfuncton, hyporeflexia (late in the
course of diseases). The rest (higher cortical function,
cerebellar, sensory, pathologic reflexes) are normal.
MOTOR WEAKNESS - LOWER MOTOR NEURON SYSTEM
• Remember that the LMN starts from the anterior horn cells -
> nerve root -> nerve plexus -> peripheral nerves -> NMJ ->
muscle
 PATTERNS OF PNS LESIONS • NMJ: ocular (ie. ptosis and diplopia), bulbar (ie. dysphagia,
• Patterns are characterized based on (1) primary dysphonia), generalized (mainly PROXIMAL, can do
characteristic/hallmark symptom, (2) sensory pattern, (3) various tests during neurologic examination: hold out arms,
motor pattern, (4) reflexes, (5) atrophy, and (6) special look up, single breath counting test)
features • Muscle: proximal as seen in myositis (eg. Inclusion Body
• Based on HALLMARK/PRIMARY CHARACTERISTICS: Myositis)
Motor Neuron Disease UMN/LMN signs • Based on REFLEXES:
Nerve Root PAIN Motor Neuron Disease HYPER/HYPOREFLEXIA
Peripheral Nerve DISTAL>PROXIMAL Nerve Root MYOTOMAL
Neuromuscular Junction FATIGABILITY Peripheral Nerve DISTAL
Muscle PROXIMAL>DISTAL Neuromuscular Junction NORMAL
• Motor Neuron Disease (eg. ALS): affects distal and Muscle NORMAL (but if severe,
proximal muscles (ie. test distal muscles by asking patient hyporeflexia)
to WALK DOWN THE STAIRS, test proximal muscles by • Motor Neuron Disease: mixture of hyper/hyporeflexia due
asking patient to WALK UP THE STAIRS), usually starting to UMN and LMN lesions
out as ASYMMETRIC then becomes symmetric later on • Nerve Root: usually ASYMMETRIC, test the important
when affectation has become severe. reflexes (Biceps – C5/C6, Triceps – C6/C7, Brachioradialis
• Nerve Root (eg. Sciatica): causes pain plus myotomal – C5/C6, Patellar – L2/L3/L4, Ankle – S1/S2)
weakness and usually affects the cervical or lumbosacral • Peripheral Nerve: usually SYMMETRIC since metabolic
area since the area of C5-C7 and L5-S1 are the peak of problems will equally affect both sides
curvatures of the spine. • Based on ATROPHY:
• Peripheral Nerve (eg. Diabetic Polyneuropathy): distal Motor Neuron Disease Depending on which is WEAK
muscles affected first because it affects the longest Nerve Root MYOTOMAL
nerves first, which are found in the foot (ie. ask patient to Peripheral Nerve DISTAL
remove shoes to check for any atrophy) Neuromuscular Junction Normal
• NMJ (eg. Myasthenia Gravis): characteristic fatigability due Muscle PROXIMAL
to limited supply of neurotransmitters from the nerve PSEUDOHYPERTROPHY
terminal. Patients start out (during the day) having good • Pseudohypertrophy is the accumulation of fat and fibrous
muscle strength (5/5 upon testing) then declines (during the tissue that replaces atrophied muscle fibers.
late afternoon and night time).
• Muscle (eg. Polymyositis): affectation of the proximal • Based on SPECIAL FEATURES:
muscles maybe due to muscle bulk (in comparison to distal Motor Neuron Disease FASCICULATIONS
muscles) Nerve Root None
• Based on SENSORY PATTERN: Peripheral Nerve CONTRACTURES
Motor Neuron Disease NORMAL Neuromuscular Junction None
Nerve Root DERMATOMAL Muscle MUSCLE PAIN AND
Peripheral Nerve DISTAL>PROXIMAL TENDERNESS
Neuromuscular Junction NORMAL • Pseudohypertrophy is the accumulation of fat and fibrous
Muscle NORMAL tissue that replaces atrophied muscle fibers.
• Seen only in diseases that mainly affect the nerve root and • Tests used to diagnose different LMN lesions: EMG-NCV,
peripheral nerve. Why? It is because these components Spine X-ray/MRI (nerve root), Fasciculation Potentials
contain sensory fibers. Recall that nerve root and (Peripheral Nerve), Repetitive Nerve Stimulation (NMJ),
peripheral nerves contain a mixture of both motor and Blood Creatine Phosphokinase (Muscle)
sensory fibers.
• Nerve Root: presents as a DERMATOMAL distribution PERIPHERAL NEUROPATHY
(remember the important dermatomes: C5-C6-C7-C8-T1- • Entrapment Neuropathies include Carpal Tunnel Syndrome
T4-T10-L5-S4-S5). (Median Nerve), Cubital Tunnel Syndrome (Ulnar Nerve),
• Peripheral Nerve: presents usually in metabolic diseases Saturday Night Palsy (Radial Nerve), Lateral Femoral
such as DM and in a STOCKING-GLOVE distribution (ie. Cutaneous Nerve Injury, Common Peroneal Nerve Injury
numbness starts in the foot due to longer peripheral nerves • Carpal Tunnel Syndrome (Median Nerve): compression at
innervating the LE, usually VIBRATION first to be affected). wrist (ie. typing for long hours), confirmed by
• Based on MOTOR PATTERN: Phalen’s/Reverse Phalen’s/Tinel’s Sign, presents with
Motor Neuron Disease ASYMMETRIC (initially) atrophy of thenar muscles
Nerve Root MYOTOMAL • Cubital Tunnel Syndrome (Ulnar Nerve): compression at
Peripheral Nerve DISTAL elbow and occasionally wrist (Guyon’s Canal -> Ulnar
Neuromuscular Junction OCULAR, BULBAR, Tunnel Syndrome), confirmed by Tinel’s/Elbow Flexion,
GENERALIZED presents with atrophy of hypothenar eminence
Muscle PROXIMAL • Saturday Night Palsy (Radial Nerve): compression at spiral
• Motor Neuron Disease: Asymmetric and affects bulbar, groove of humerus, confirmed by Tinel’s, presents with wrist
upper and lower extremities drop
• Nerve Root: C5 (abduction, flexion), C6 (thumb abduction), • Meralgia Paresthetica (Lateral Femoral Cutaneous Nerve):
C7 (extension), C8 (digital abduction), L4 (knee extension), compression as the nerve passes under the inguinal
L5 (dorsiflexion, HEEL WALK), S1 (plantarflexion, TOE ligament, no motor presentation
WALK) • Common Peroneal Nerve Injury: compression at fibular
• Peripheral Nerve: weakness develops in specific head, confirmed with steppage gait, presents with foot drop.
innervations then progresses to contractures (eg. Papal
Benediction sign in ulnar nerve neuropahy)
 MOTOR WEAKNESS - UPPER MOTOR NEURON SYSTEM
• Proper reporting of the motor system: eg. Weakness is
spastic, muscles are hypertonic, hyperreflexic with no
fasciculations and atrophy
• 4 components of the motor system: (1) direct activation
pathway, (2) control circuits, (3) indirect activation pathway,
and (4) final common pathway.
DIRECT ACTIVATION PATHWAYS
• Function: to effect voluntary activity, especially skilled
conscious movements of the fingers
• Most pyramidal system neuronal cell bodies in the precentral
gyrus and anterior part of the paracentral lobule (but
some also in supplementary areas and parietal lobe)
• All axons from the motor cortex coverage toward the
POSTERIOR LIMB of the internal capsule arranged from
anterior posterior in the order of face, arm, leg, bladder and
rectum
• Tracts originate from the pyramidal cells in layer V of the
cerebral cortex, and a few from giant pyramidal cells of Betz
• Major transmitters include glutamate and GABA.
CORTICOBULBAR TRACT
• Usually the NONOCULAR brainstem LMNs are supplied
BILATERALLY by the motor area except for lower facial
muscles, which are supplied solely by the contralateral
motor area.
• Clinical correlation: central (commonly seen in MCA stroke)
and peripheral facial palsy (commonly seen in Bell’s Palsy)
• Bell’s Palsy: transient LMN lesion of CN VII believed to be
caused by a viral infection (eg. HSV) occurring at or beyond
the stylomastoid foramen resulting in the ff. symptoms:
marked facial asymmetry, atrophy of facial muscles, facial
drooping (eyebrows, mouth), uncontrolled tearing,
inability to close the eyes (remember CN VII is the efferent
limb of the corneal reflex), difficulty keeping food in mouth
(remember that CN VII also controls some muscles of
mastication), ipsilateral hyperacusis (remember that CN VII
innervates the stapedius muscle)
CONTROL CIRCUITS
• Function: to control and modify motor activity through the
CEREBELLUM and BASAL GANGLIA
• Receives input from cerebral cortex and project back via the
thalamus; Sends information to brainstem and indirect
activation pathways
• Basal ganglia: maintains background support/posture
needed for voluntary motor activity, lesions cause
hypo/hyper/dyskinesia and rigidity
• Cerebellum: coordinates/corrects movement errors of
muscles, lesion cause defects in rate, range and force of
movements
INDIRECT ACTIVATION PATHWAYS
• Function: mediate the automatic activities involved in
normal motor function (eg. maintaining proper posture) via
subconscious coordination
• Lesions usually result in abnormal muscle tone and reflexes
• 4 important pathways:
• RUBROspinal (red nucleus to spinal cord): facilitates flexor
movements of the contralateral upper extremity
• RETICULOspinal (reticular formation to spinal cord):
facilitates sensorimotor integration, postural reflexes
(pontine reticulospinal), and inhibition of segmental
muscle stretch and flexor reflexes (medullary
reticulospinal)
• VESTIBULOspinal (vestibular nuclei to spinal cord):
facilitates coordinated control of head-eyes-neck
movement for equilibrium (MEDIAL), and facilitates
extensor trunk-limb reflexes (LATERAL) critical for
maintenance of proper posture; lesion results to motion
sickness and vertigo.
• TECTOspinal (tectum in the midbrain to spinal cord):
facilitates coordinated head-eye movements
FINAL COMMON PATHWAY
• This is simply the pathway from peripheral nerve to muscle.
Motor unit consists of LMN from the anterior horn cells in the
spinal cord until the muscle. Neurotransmitter involves in
acetylcholine.
EVALUATION OF MOTOR WEAKNESS
• UMN is commonly susceptible to Vascular, Demyelinating
and Traumatic insults. Evaluation involves determining the
onset, time curse and distribution of weakness and other
associated neurologic findings. Proper reporting of findings
during motor system testing is critical.
• Common cause of focal weakness: CVD, brain tumors,
myelopathies, multiple sclerosis.
• The most frequent pyramidal tract disorder is a CAPSULAR
stroke referring to a stroke of internal capsule where the
corticospinal and corticorubral tracts converge and pass
through producing symptoms of paralysis of the contralateral
lower face, upper and lower extremities.
• Temporal Pattern of Neurologic Symptoms
• Within minutes or less -> trauma or vascular etiology
• Over hours to days -> acute or subacute disorders such
as cord compression, myelitis, GBS
• Over weeks to months -> subacute or chronic disorders
such as inherited polyneuropathies, myasthenia gravis,
tumors, myelopathies
• Fluctuates from day to day -> metabolic myopathies and
multiple sclerosis
• Fluctuates over course of the day -> myasthenia gravis
• Anatomic Weakness Pattern
• PROXIMAL weakness -> difficulty in reaching upward,
going up the stairs
• DISTAL weakness -> difficulty in movements requiring fine
dexterity such as holding an object, writing, buttoning
• BULBAR weakness -> cranial nerve deficits
• Do a systematic and complete neurologic examination to
guide your diagnostic approach (eg. MRI, vascular studies,
lumbar puncture, EEG)
• Spinal lesions commonly result in a sacral sparing
phenomenon due to somatotopic localization. Complete
transection results in functional abnormalities below the
lesion (voluntary movements, sensations, reflexes).
• Level of transection
• C5 above: respiratory difficulty
• C7 or above: quadriplegia
• C8-T1: paraplegia and weakness of the hands
• Thoracic and Lumbar: paraplegia
• *Acute cervical/high thoracic lesions (usually trauma):
sympathetic/neurogenic shock (transient hypotension,
miosis, bradycardia but more permanent incontinence and
impotence)
• Lesion in the area of decussation: weakness of
contralateral upper extremity-ipsilateral lower extremity
(CRUCIATE paralysis)
• Remember the mnemonic VITAMIN CDEF for differential
diagnosis.
ALTERED SENSORIUM AND SYNCOPE
• Consciousness is a state of full awareness of the self and
one’s relationship to the environment.
• Sensorium is our awareness. Comatose is state of
incapability to be aroused by stimuli or inner need
 COMA AND ALTERED SENSORIUM
• State of consciousness controlled by the ARAS spanning the
brainstem reticular formation projecting to the thalamus,
hypothalamus and cortex. Hence, we can surmise that a
comatose patient has a lesion in the BRAINSTEM LEVEL
OR ABOVE.
• Neurotransmitters involved include acetylcholine
(pedunculopontine tegmental and laterodorsal tegmental
nuclei), norepinephrine (locus ceruleus), serotonin (dorsal
and median raphe nuclei), dopamine (ventral periaqueductal
grey matter) and histamine (tuberomammillary nucleus)
• Cause is usually STRUCTURAL (asymmetric, focal findings
with abnormal reflexes) versus METABOLIC (symmetric and
non-focal findings with normal reflexes
EVALUATION, EXAMINATION AND APPROACH TO COMA
• Remember S-P-E-R-M: Sensorium – Pupils – EOMs –
Respiration - Motor
• Levels of Consciousness: elicited by using visual, auditory
and noxious stimuli
• AWAKE: oriented to time, place and person
• DROWSY (aka SOMNOLENT/LETHARGIC): dozes off
while responding to stimuli but can still follow simple
commands
• OBTUNDED (aka mentally dulled): decreased interest in
surroundings, slow responses, short arousal periods,
unable to follow any commands
• STUPOROUS: responds with noxious stimuli by
grimacing/drawing away
• COMATOSE: no response to any stimuli, no verbal output,
with either decorticate/decerebrate posturing
• Pupillary Reflex (from superior to inferior)
• SMALL, REACTIVE: lesion possibly at diencephalon, but
most commonly due to diffuse effects of drugs and
metabolic encephalopathy
• ANISOCORIA: lesion at CN III, commonly caused by uncal
herniation
• MIDPOSITION, FIXED: lesion at midbrain
• PINPOINT: lesion at pons
• EOMs: elicited by the oculocephalic reflex and cold calorics
• Oculocephalic (Doll’s Eye) reflex: normally inhibited and is
released from inhibition during coma, results in conjugate
movement of the eyes in the opposite direction, which is
elicited by turning/tilting the head. Afferent arm from the
labyrinth, vestibular nerve and neck proprioceptors.
Efferent arm from the CN III-IV-VI and EOMs. Absence of
the doll’s eye reflex in a comatose patient likely points to a
lesion in the area of the afferent and efferent arms.
• Cold Calorics: normally, cold water causes slow phase
towards the ipsilateral ear and a corrective fast phase
towards the opposite ear, this is lost in comatose patients.
Remember that only the SLOW PHASE IS
LOCALIZABLE. Note that COWS is not a very good tool
for localization. Absence of cold calorics in a comatose
patient likely points to a lesion in the area of pons, medulla,
CN III-IV-VI and CN VIII.
• *Other cranial nerves for localization value: corneal reflex
test (for CN V), grimace and response to pain (for CN VII),
gag reflex (for CN IX-X)
• Respiratory (from superior to inferior, based on breathing
patterns)
• CHEYNE-STOKES (waxing and waning episodes of
hyperpnea with apnea in between): caused by isolation of
brainstem respiratory centers from the cerebrum, lesion
most likely at the bilateral cerebral hemispheres
• CENTRAL NEUROGENIC HYPERVENTILATION
(increased rate and depth of respiration enough to cause
respiratory alkalosis): caused by release of reflex
mechanisms for respiratory control in the lower brainstem,
lesion most likely at the lower midbrain-upper pontine
tegmentum
• APNEUSIS (pause of 2-3 seconds in full inspiration):
caused by basilar artery occlusion, lesion most likely at the
lower pons
• CLUSTER BREATHING (few rapid deep breaths
alternating with apneic episodes): lesion most likely at the
lower pons
• ATAXIC/BIOT’S BREATHING (irregular breath patterns
with variable rate and depth): lesion most likely at the
dorsomedial medulla
• Motor
• Examiner must do manual muscle testing, reflexes and
pathologic reflexes.
• Classic findings include clasp knife rigidity, (+) Babinski
• GLASGOW COMA SCALE: lowest score – 3, highest – 15
• E4-V5-M6, important to master GCS scoring!
• Known Causes of Coma include STRUCTURAL,
METABOLIC and PHYSIOLOGIC causes
• Structural: TBI, SAH, ICH, CVD Infarct, Tumor, Infection
• Metabolic: Hypoxia, Hypercarbia, Fluid and Electrolyte
Disorders, Endocrine Abnormalities, Toxins, Vitamin
Deficiency, requires good neurologic examination and EEG
• Physiologic: Non-convulsive seizures, requires STAT EEG
• *Lab tests: blood tests, ABG, urinalysis, CSF analysis
• If cause if Unknown, examiner may opt for a cranial CT/MRI
(if abnormal – likely structural; if normal – likely metabolic,
hence do EEG)
• Monitoring acute organ injuries as likely causes of coma is
critical
• Why do EEG monitoring even when known structural and
metabolic causes, and known seizures have been controlled?
To rule out subclinical seizures which do not present with
convulsions since these can cause coma.
SYNCOPE
• TRANSIENT and RAPID loss of consciousness with inability
to maintain postural tone followed by SPONTANEOUS
RECOVERY
• Most common causes include cardiac (arrhythmia,
structural), non-cardiac (vasovagal, orthostatic,
cerebrovascular). This must be differentiated against non-
syncopal attacks
• CARDIAC: (1) arrhythmias (more common during exertion or
supine, with palpitations at the time of syncope), (2)
structural; evaluation includes complete Hx/PE and 12-L
ECG
• NON-CARDIAC: (1) nerually mediated (caused by
inappropriate vagal/sympathetic tone, with characteristic
prodrome of increased warmth/cold, fatigue,
lightheadedness, sweating and nausea, precipitated by
stress, trauma, pain, sight of blood and prolonged standing,
and rapid recovery with headache, fatigue and weakness,
types further subdivided into carotid sinus, situational faint
and classic vasovagal), (2) orthostatic hypotension (caused
by insufficient autonomics to counter the drop in cardiac
output during upright posture), (3) cerebrovascular (caused
by basilar stroke, but almost never the cause of true
fainting)
• NON-SYNCOPAL ATTACKS: categorized into disorders with
loss of consciousness (metabolic, epilepsy, TIA, intoxication)
and without loss of consciousness (psychogenic, TIA)
EVALUATION, EXAMINATION AND APPROACH TO
SYNCOPE
• History must include events before, at the onset, during, and
after the attack
 • Events before: position (supine/sitting -> ARRHYTHMIA; • Positive sensory symptoms: dysesthesia, allodynia,
exertion -> STRUCTURAL), activity, situation, risk factors hyperpathia
(prolonged standing -> VASOVAGAL; coughing-urination- • Negative sensory symptoms: anesthesia, hypoesthesia
defecation -> SITUATION; head rotation-neck movements - • Nerve Proper
> CAROTID SINUS; sudden standing from lying position -> • Generalized polyneuropathy: axonal (metabolic, toxic),
ORTHOSTATIC), triggers demyelinating (GBS)
• Events at the onset: w/ prodrome -> NEURALLY- • Focal neuropathy: such as the previously mentioned
MEDIATED w/o prodrome -> ARRHYTHMIA, entrapment neuropathies
• Events during: falling quickly -> ARRHYTHMIA, kneeling • Multifocal neuropathy: bilateral and asymmetric, such a in
over -> VASOVAGAL, brief and w/ Hx of heart disease -> Leprosy (Hypopigmented patches d/t infectious neuritis)
ARRHYTHMIA, >4-5 mins -> SEIZURE, METABOLIC, • Nerve Root
VASOVAGAL, tonic-clonic before falling -> SEIZURE, • Remember the characteristic PAIN in nerve root problems
tonic-clonic after falling -> VASOVAGAL, tongue biting -> • Most commonly due to disc herniations in the cervical and
SEIZURE lumbosacral region, can also affect thoracic region (eg.
• Events after: palpitations or waking up feeling normal -> HZV lying dormant in the dorsal root ganglion)
ARRHYTHMIA, chest pain -> STRUCTURAL HEART • Cauda Equina Syndrome (prolapse of central disk at L4-L5
DISEASE, nausea/vomiting/weakness/fatigue -> and L5-S1 manifesting as bilateral leg pain/weakness, saddle
VASOVAGAL, incontinence -> SEIZURE, anesthesia, bowel/bladder symptoms, impotence)
headache/diplopia/hemiparesis -> TIA/STROKE • Versus. Conus Medullaris Involvement: Sacral Sensory
• Others: medications, prior episodes (if >1 over multiple Sparing
years -> BENIGN, if >1 over short period of time -> • Sensory Neuropathies
SERIOUS CAUSE and likely ARRHYTHMIA), family history
• Types: complete transection, tabetic syndrome
of unexplained sudden death, past history of cardiac
(posterior column lesion), Brown-Sequard syndrome
disease/seizures/DM/alcohol intoxication
(hemitransection), syringomyelic syndrome (cystic spinal
• Physical Examination: cord mass from C4-T4, causing weakness of hands and
• Vital signs: check BP while supine for 5 minutes then after cape-like numbness), posterior column syndrome
standing for 3 minutes, if SBP/DBP falls by >20/10 mmHg - (posterior spinal artery occlusion causing loss of position
> ORTHOSTATIC SYNCOPE sense, hypoesthesia, ataxia and asynergia), anterior
• Heart: check for signs of heart failure/pulmonary embolism spinal artery syndrome (causes loss of motor function
• Lungs: check for PMI and murmurs and loss of pain and temperature sensation)
• Neurologic Examination: r/o focal findings suggestive of
stroke DIZZINESS AND DYSEQUILIBRIUM
• Diagnostic tests: cardiac (needs work-up, ECG, 2D Echo,
Stress Test, Holter), neurologic (does not require work-up, VESTIBULAR SYSTEM
may do EEG, tilt table testing) • Remember the structures: bony and membranous labyrinth, 3
semicircular canals (for angular acceleration, gaze stability,
SOMATOSENSORY DISORDERS with crista ampullaris), otoliths (for linear acceleration,
postural stability, with maculae acusticae)
CENTRAL COMPONENTS • Vestibular pathways include lateral and medial
• Remember the pathway of the DCML and the somatotopic vestibulospinal tracts
localization of the nucleus/fasciculus gracilis (more medial) • Vestibular connections with other systems include the ff:
and nucleus fasciculus cuneatus (more lateral). Lesions • MLF – for vestibulo-ocular reflex – for eye movement
result in the following symptoms: • Cerebellum – for vestibulospinal reflex – for coordination
• Loss of position and movement sense, two-point and timing of movement
discrimination, astereognosis and agraphesthesia, (+) • Neck – for vestibule-collic reflex – associated with neck
Romberg’s sign movements
• Remember the pathway of the ALS, which includes the
spinothalamic tract, spinoreticular tract and DIZZINESS, VERTIGO, PRESYNCOPE, DYSEQUILIBRIUM,
spinomesencephalic tract, and the somatotopic localization of AND LIGHTHEADEDNESS
the fibers from the upper limbs and trunk (more medial) and • Categories of dizziness include vertigo (to and fro or up and
lower limbs (more lateral). Lesions result in the following down movement of the body, most commonly PERIPHERAL
symptoms: in origin), disequilibrium (veering to one side), presyncope
• Loss of pain, temperature and crude touch (faintness sensation), lightheadedness (giddiness,
• Both ALS and DCML terminate in the VPL nucleus and accompanies anxiety, usually IDIOPATHIC/PSYCHIATRIC)
posterior nuclear group in the thalamus. • Important characteristics in dizziness: timing, triggers and
telltelate signs (to rule out acute vestibular syndrome at risk
PERIPHERAL COMPONENTS for stroke)
• Receptor organs: converts physical and chemical changes in • Important to differentiate PERIPHERAL vs. CENTRAL
the environment into electrical impulses that can be causes of vertigo:
processed by the CNS (transduction) PERIPHERAL CENTRAL
• Skin receptors have two classes: free nerve endings (for Focal deficits (-) (+)
pain and temperature) and encapsulated end organs (for Deafness (+) (-)
fine touch, 2-pt discrimination, vibration and pressure sense
Tinnitus (+) (-)
• Nociceptors usually made up of A-delta (light touch, sharp
Nytagmus Fast phase is Fast phase
and pricking pain) and C fibers (slow and burning pain) opposite the towards opposite
• Mechanoreceptors usually made up of A-alpha (limb lesion, (+) fixation side, (-) fixation
proprioception), A-beta (joint capsule pressure, flutter, suppression suppression
vibration, pressure) Latency 1-40 s None
 Duration Few minutes Persistent
Intensity Severe Mild
Systemic Marked nausea Less intense
Symptoms and vomiting nausea and
vomiting
• Causes of PERIPHERAL Vertigo:
• BPPV: caused by detachment of otolithic crystals and
reattachment to posterior semicircular canal (most
commonly), characterized by paroxysmal vertigo and
nystagmus especially on CHANGES IN POSITION, lasts
less than a minute but recurs periodically, diagnose by DIX-
HALLPIKE Maneuver
• Meniere’s: caused by increase in endolymph volume and
distention of the endolymphatic system with rupture of
membranous labyrinth and dumping of potassium-
containing endolymph into perilymph, characterized by
recurrent attacks of vertigo, tinnitus, deafness for minutes
to hours with nausea/vomiting/tendency to fall towards
affected ear.
• Labyrinthitis: caused by bacterial/viral infection of the
superior part of the vestibular nerve trunk, characterized by
paroxysmal but prolonged (hours to days) single attack of
vertigo
• Toxic Bilateral Vestibulopathy: caused by prolonged
exposure to aminoglycosides and other ototoxic
substances, characterized by disequilibrium
• Causes of CENTRAL Vertigo:
• Acoustic Neuroma: caused by space-occupying lesion
presenting in the cerebellopontine angle, characterized by
high-frequency deafness, tinnitus, mild chronic imbalance
associated with headache, CN V-VII-X palsies, and
ipsilateral ataxia
• Labyrinthine Infarction: caused by occlusion of the AICA
and labyrinthine division of the internal auditory artery,
characterized by single abrupt attack of vertigo, nausea,
vomiting without tinnitus or hearing loss.
• Brainstem Vertigo: caused by vascular, demyelinating and
neoplastic lesions that affect the vestibular nuclei and its
connections, characterized by marked nystagmus without
vertigo associated with cranial nerve, sensory and motor
system involvement
• Dysequilibrium usually d/t multisensory deficit, decreased
visual acuity, peripheral neuropathy, Parkinson’s.
• Lightheadedness usually categorized as psychiatric or
idiopathic types.
EVALUATION, EXAMINATION AND APPROACH
• History: description and type of the dizziness, positional
effects, otologic-neurologic-psychiatric symptoms
• Physical Examination: Vital signs (for orthostasis), hearing,
cardiac, neurologic (especially gait), Dix-Hallpike test
(master/familiarize how to do this test), Head Thrust test
(used to assess vestibule-ocular reflex), Calorics testing
• Results of the Dix-Hallpike Maneuver:
• Central lesion: pure vertical and downbeat nystagmus
• Peripheral lesion horizontal and upbeat/torsional
nystagmus (BPPV), unidirectional and horizontal
(labyrinthitis)
• Further testing to rule out other categorizes of dizziness and
their causes.
EPILEPSY AND OTHER SEIZURE DISORDERS
• Seizure is a transient and reversible alteration of behavior
caused by a paroxysmal, abnormal and excessive neuronal
discharge, common manifestation of neurologic diseases
• Epilepsy is two or more seizures not directly provoked by
intracranial infection, drug withdrawal, acute metabolic
changes of fever.
SEIZURE VERSUS EPILEPSY
• Causes vary by age group: neonates (hypoxic ischemic
encephalopathy, congenital malformations, infections),
infants (fever, infections, post-hemorrhagic sequelae),
childhood (genetic disorders, trauma, neoplasm), young
adults (idiopathic, trauma, drug withdrawal), middle-aged
adults (trauma, neoplasm, vascular disease), old-aged
(vascular disease, tumor, degenerative disease)
• Most common in INFANTS and ELDERLY
• Differentials for seizures: SYNCOPE, pseudoseizures,
breath holding spell, sleep disorders, movement disorders
• Provoked seizures: fever, sleep deprivation, hyponatremia,
hypoglycemia, hypoxia, drug/alcohol withdrawal
• CONVULSIONS: most common manifestation of seizures
• Partial – occur in focal brain regions (most commonly frontal
and temporal lobes)
• Simple Partial: caused by focal cortical discharge,
characterized by motor, somatosensory, autonomic,
psycho-cognitive symptoms, generally brief and (-) LOC
• Complex Partial: caused by focal discharge from temporal
lobe, characterized by behavioral arrest followed by
staring, automatisms and postictal confusion, and (+) loss
of awareness
• Secondarily Generalized: caused by partial seizures
evolving to secondarily generalized seizures
• Generalized – occur in bilateral cerebral hemispheres
• Absence (Petit Mal): common in children, characterized by
sudden and brief lapse of consciousness, motionless blank
stares but (-) loss of postural tone, EEG shows 3-Hz
spike and wave pattern
• Myoclonic: characterized by sudden and brief shock-like
contractions during wakefulness (physiologic myoclonus
or hypnic jerks can occur during sleep), EEG shows
bilaterally synchronous spikes or polyspikes and
waves
• Clonic: characterized by muscle spasms and bilateral jerks
followed by rapid relaxation, EEG shows rapid spikes
with slow waves
• Tonic: characterized by sudden, brief but sustained
contraction of extensor axial muscles and limb muscles
with LOC, EEG shows rapid spikes
• Atonic: mistaken for fainting/syncope, characterized by
sudden loss of postural muscle tone with great risk for
head injury, EEG shows brief and generalized spike and
wave discharges followed by diffuse slow waves
• Tonic-Clonic (Grand Mal): most common seizure type
resulting from METABOLIC DERANGEMENTS,
characterized by initial motor signs (brief trunk flexion,
opening of mouth and eyelids, upward eye deviation) ->
tonic phase (extension of back, neck, arms and legs, ictal
cry d/t respiratory muscle spasm, tongue biting, dilated and
unreactive pupils, incontinence) -> clonic phase (flexor
spasms, eye blinking, salivary frothing, cyanosis, prominent
autonomic signs) -> terminal phase (deep coma, entire
body is limp)
• Epilepsies
• Localization to specific cortical lobes possible or can be
generalized.
• Generalized: can be idiopathic (genetic in origin, with (+)
FHx, begins early in life and BENIGN PROGNOSIS),
secondary (structural cause identified usualy stroke, tumor
or trauma and mental retardation may occur), cryptogenic
(structural cause suspected but cannot be identified)
• Pathogenesis: shift of normal balance of excitation and
inhibition of the CNS (precipitated by hyperexcitable
neurons, high GLUTAMINE, low GABA)
 EVALUATION, EXAMINATION AND APPROACH
• History: onset, presence of aura, ictal manifestations, diurnal
variation, triggering factors (flickering lights, alcohol,
medications, stress, fever, sleep deprivation), frequency,
seizure-free periods, injuries, frequency of ER consults.
• SEIZURE vs. SYNCOPE
SEIZURE SYNCOPE
Injury Common Rare
Incontinence Common Rare
Post-ictal confusion Common Rare
Headache Common Rare
Focal deficit Occassional Rare
Relation to Posture (-) (+)
Prodrome Short long
• Diagnosis: CLINICAL diagnosis, requires accurate
eyewitness account, but EEG is the single most important
diagnostic procedure for confirming the diagnosis of epilepsy,
MRI to rule out secondary causes
• Other tests: CBC, RBS, blood chemistry, ECG, creatine
kinase
• Treatment: AED only if RECURRENT or until a SECOND
SEIZURE occurs (can only prevent seizures and most
importantly, STATUS EPILEPTICUS), MONOTHERAPY is
the recommended choice and choice depends on type of
seizures/epilepsy syndrome
• Tonic – Clonic: Carbamazepine, Phenytoin, Valproic
Acid, Phenobarbital
• Clonic: Valproic Acid
• Absence: Valproic Acid, Ethosuximide
• Myoclonic: Valproic Acid, Clonazepam
• Atonic: Valproic Acid
• Goal of therapy: complete seizure control, monotherapy
and minimal side effects
• Start therapy: definite diagnosis, risk of recurrence, weight
risk/benefits for pregnany women
• Discontinue therapy: 3-5 years of complete control, normal
neurologic examination and normal EEG
• Other interventions: epileptic surgery (for intractable
epilepsies), ketogenic and medium chain triglyceride diet
(augments GABA effects but high in fat)
• STATUS EPILEPTICUS: recurrent generalized convulsions
at a frequency that prevents regaining of consciousness
in the interval between seizures, prolonged convulsive
status (>5 mins) but by definition it is specified to be at 15-20
minutes.
• Medications given: Diazepam, Phenytoin, Phenobarbital
• If all else fails: ANESTHESIZE!
HEADACHE AND CRANIOFACIAL PAIN
• Approach to headache includes differentiating primary versus
secondary headache. Most common are the primary benign
types (90%).
• Important to note the pain-insensitive structures (includes
basically everything within the brain parenchyma from the
ventricular ependymal, choroid plexus and pial veins)
HEADACHE
• Two types of headache include primary (no exogenous
cause) and secondary (with exogenous cause).
• Primary types of headache include Migraine, Cluster
Headache, and Tension Headache. Secondary types of
headache include those caused by trauma, vascular
disorders, metabolic, infection and psychiatric disorders.
EVALUATION, EXAMINATION AND APPROACH
• History/PE is always critical. Cardinal features should include
OLD CARTS.
• Ruling out secondary causes, especially life-threatening
causes (eg. SAH described “worst headache of my life”)
• Red flags for headache include the following:
• First-ever attack of headache
• Sudden and explosive headaches
• Associated eye signs
• Fever, Altered mentation/level of consciousness
• Change in character of the headaches
• Prior conditions
• *The mnemonic SNOOPS is used: Systemic symptoms,
Neurologic symptoms, Onset, Old age, Prior history,
Secondary illness
• Headaches requiring consultation:
• Severe, or “worst headache of your life”
• Subacute headache with increasing frequency and severity
• Aggravated by exertion, coughing, bending, coitus
• Persistently on the same side
• Awakens patient at night or disrupts sleep
• Associated with fever, stiff neck, blurred vision, slurred
speech, weakness and confusion
• No response to standard treatment
• Disabling and interfering with quality of life and activities of
daily living.
MIGRAINE
• Begins in childhood/adolescence/early adulthood, more
predominantly seen in women
• Characteristic: periodic, predominantly unilateral, often
pulsatile/throbbing headaches.
• Pathophysiology: Spreading Cortical Depression (causing
dysfunction of brainstem serotonergeric and noradrenergic
pain pathways)
• Diagnostic Criteria (ICHD-3) for Migraine WITHOUT AURA
• (A) At least 5 attacks fulfilling Criteria B-D
• (B) Headaches lasting 4-72 hours
• (C) At least 3 of the following 4 characteristics: unilateral,
pulsatile, moderate or severe pain, aggravation by routine
physical activity
• (D) During headache, at least one of the following: nausea,
vomiting or both, and photophobia and phonophobia
• Diagnostic Criteria (ICHD-3) for Migraine WITH AURA
• (A) At least 2 attacks fulfilling Criteria B
• (B) At least 3 of the following 4 characteristics: (1)
one/more of the following fully reversible aura symptoms
indicate focal cerebral cortical/brainstem dysfunction, (2) at
least 1 aura symptoms develops gradually over >/= 4
minutes or >2 occur in succession, (3) No aura symptoms
last > 60 minutes, (4) H/A follows aura with a free interval of
<60 minutes.
• Treatment: NSAIDs (mild/moderate attacks), Triptans (severe
attacks)
CLUSTER HEADACHE
• Predominant in men
• Characteristic: cluster pattern attacks, consistently unilateral
orbital localization with nightly recurrence, between 1-2 hours
after onset of sleep or several times during the night
(nocturnal headache)
• Pathophysiology (mostly theoretical): dysfunction of CN V
with hypothalamic mechanism related to the characteristic
nightly recurrence
• Associated vasomotor phenomena (unilateral): bulging and
pulsating temporal artery, unilateral ptosis-swelling and eyelid
redness, miosis and conjunctival injection, tearing, nasal
congestion and rhinorrhea, facial flusing and sweating.
• Treatment: ergotamine, triptan, verapamil
 TENSION HEADACHE
• Most common headache variety. More likely to occur in
middle age and coincides with anxiety, fatigue and
depression
• Characteristic: bilateral, with occipitonuchal, temporal, or
frontal predominance, or diffuse extension over the top of the
cranium, dull and aching/fullness/tightness/pressure; lasts for
longer periods of time
• Pathophysiology: excessive contraction of craniocervical
muscles and associated constriction of scalp arteries
• Treatment, analgesics (relief for brief periods only), massage,
meditation and biofeedback techniques
OTHER PRIMARY HEADACHE SYNDROMES
• Idiopathic Stabbing Headaches: similar to Cluster headache
but without associated vasomotor phenomena
• Cold Stimulus Headache/Ice Cream Headache: short-lasting
moderate to severe pain in the palate and throat, bilateral
headache and self-limited
• Benign Cough Headache: “bursting” pain usually in the
frontal and occipital area, unilateral/bilateral, usually following
coughing/sneezing
• Benign Exertional Headache: episodes of bilateral, pulsatile
headache triggered by physical exercise
• Coital Headache: dull and bilateral headache increasing as
sexual increases and may evolve to severe throbbing and
explosive headache at the time of orgasm.
• Occipital Neuralgia: paroxysmal pain in the area of
distribution of the greater and lesser occipital nerves
CEREBROVASCULAR DISEASE
• Stroke is a rapid loss of brain function due to blood supply
disturbance to the brain, persisting beyond 24 hours. Brain
requires 50-55ml/100g brain tissue/min
• TIA is a focal neurologic deficit lasting less than 24 hours
• EMERGENCY, PREVENTABLE, TREATABLE!
• Warning signs: SUDDEN, FOCAL (weakness, numbness,
loss of speech, loss of comprehension, slurring of speech,
loss of vision, headache, dizziness, loss of balance)
• Basic pathophysiology: vascular occlusion -> loss of oxygen
and glucose supply -> activation of phospholipases ->
neuronal membrane function alteration -> excitotoxicity
• Diagnosis: establish TIME OF ICTUS, do a PLAIN CRANIAL
CT SCAN
• Differential Diagnosis: r/o common stroke MIMICKERS
(seizures, tumor, vertigo, syncope, dementia, bell’s palsy,
hypertensive encephalopathy, dementia), recognize common
stroke CHAMELEONS (movement disorders – basal ganglia
stroke [chorea -> putamen, ballimus -> subthalamic nucleus,
athetosis -> globus pallidus; agitation and delirium – temporal
lobe stroke; sensory symptoms – parietal lobe affectation;
cortical blindness – occipital lobe affectation)
• After ruling out other DDx, differentiate stroke subtypes,
check eligibility for thrombolytic therapy (if ischemic stroke)
then screen out complications of stroke
• Assessment: stabilize, monitor vital signs, general medical
assessment (patient history, onset), neurologic examination
(GCS, NIHSS), plain cranial CT Scan
• Therapy: 3-4.5 hours is the golden hour in acute stroke, goal
is to save the ischemic PENUMBRA (UMBRA is the core
infarct while OLIGEMIA is an area that surrounds the
penumbra) via recanalization (through thrombolytic therapy
with rTPA) and neurovascular protection (physiologic and
pharmacologic means)
• Critical values: blood flow <70% - oligemia, <40% - electrical
disturbances, <20% - potential disturbances, <10% - death
• Critical time periods: Door to Doctor (10 mins), to CT
completion (25 mins), CT scan reading (45 mins), treatment
(60 mins), neurology expertise (15 mins), neurosurgery
expertise (2 hours), monitored bed (3 hours)
ISCHEMIC STROKE
• Most common type of stroke with embolic strokes being the
most common type of ischemic stroke
• Types: atherothrombotic (less sudden), embolic (sudden,
usually cardioembolic in origin, most frequently involving the
MCA), lacunar (<1cm, involves small penetrating branch
arteries)
HEMORRHAGIC STROKE
• Classically presents with sudden onset of LOC, very severe
headache, vomiting, seizures along with the focal deficits.
• Types: intracerebral (most commonly affects putamen and
internal capsule), subarachnoid (usually due to saccular
aneurysm rupture)
CLINICAL STROKE SYNDROMES
• Anterior Cerebral Artery – A1 usually well tolerated due to
adequate collateral flow from contralateral ACA. A2
affectation usually results in the following deficits:
• Contralateral weakness (LE>UE and face)
• Contralateral numbness (LE>UE and face)
• Bladder Incontinence
• Sympathetic apraxia and frontal release signs
• Middle Cerebral Artery – most common site for embolic
strokes, especially affecting the branching arteries supplying
the basal ganglia and internal capsule.
• M1 affectation – Contralateral weakness (UE and face >
LE), Contralateral weakness of the lower half of the face,
Contralateral hemisensory loss (UE and face > LE) and
hemineglect, Global aphasia, contralateral homonymous
hemianopsia, gaze deviation towards side of the lesion
• Superior division affectation – Contralateral weakness (UE
and face > LE), Contralateral weakness and numbness of
the lower half of the face, Contralateral hemisensory loss
(UE and face > LE), Broca’s aphasia
• Inferior division affectation – Contralateral homonymous
hemianopsia, Contralateral upper quadratonopsia,
Contralateral constructional apraxia, Wernicke’s aphasia
• Posterior Cerebral Artery – different syndromes exist such
as the ff:
• Unilateral occipital affectation – homonymous hemianopsia
• Bilateral occipital affectation – Anton’s Syndrome (bilateral
homonymous hemianopsia, visual anosognosia)
• Weber syndrome – contralateral weakness of the
extremities with ipsilateral CN III lesion (ptosis, dilated
pupil)
• Vertebral Artery – includes PICA lesion (Lateral
Medullary/Wallenberg Syndrome) manifesting with the ff:
• Contralateral hemisensory loss
• Ipsilateral Ataxia
• Ipsilateral facial numbness
• Ipsilateral palatal, pharyngeal and vocal cord paralysis,
Singultus (persistent hiccups)
• Persistent vertigo, nystagmus
• Basilar Artery – mainly CROSSED SYMPTOMS d/t
brainstem affectation and includes several syndromes such
as the ff:
• Top Basilar – (+) transient LOC, hemianopsia, bilateral
ptosis, pupillary enlargement with preserved pupillary light
reflex
• Midbasilar (Locked-in Syndrome) – (-) LOC, quadriplegia,
CN IV-VI palsy
• AICA (Lateral Pontine, Marie-Foix Syndrome) –
contralateral weakness and numbness, ipsilateral ataxia,
ipsilateral facial numbness/weakness
 SAMPLE QUESTIONS Question 7. A 65-year old patient comes to your clinic for
follow-up consult of a previous cerebrovascular disease that
Question 1. A 40-year old female comes to your clinic occurred years ago. On neurologic examination, you ask the
complaining of blurring of vision of the left eye since 6 months patient to speak a sentence but you observe exorbitant effort in
prior to consult. She has been having progressively trying to speak. This patient most likely had a cerebrovascular
worsening headache, irregular menstruation and galactorrhea infarct of which part of the cerebral cortex?
as well. Upon consult, she now has blurring of vision on the A. Superior Frontal Lobe
right eye, saying to you that she feels like she has tunnel-like B. Inferior Frontal Lobe
vision. What is correct term for the patient’s chief complaint? C. Superior Temporal Lobe
A. Biparietal Hemianopsia D. Inferior Temporal Lobe
Answer: B. This is Broca’s aphasia, characterized by partial loss of the ability to speak written/spoken words.
B. Bitemporal Hemianopsia Effortful speech is observed, with comprehension usually remaining intact.

C. Bitemporal Homonymous Hemianopsia

Question 8. A 12-year old boy with above average
D. Biparietal Homonymous Hemianopsia
Answer: B. This is a case of pituitary adenoma. Key word is “tunnel-like vision”. This is not usually stated by the intelligence, while playing with his friends near the staircase of
patient but a description that must be elicited by the clinician. Progressively worsening and chronic headache
strongly supports a neoplastic lesion while irregular menstruation and galactorrhea are symptoms of
their school, fell from the stairs. Head injury followed the fall but
hyperpituitarism caused by the overgrowth of functional cells of the pituitary gland. no consult was done for fear of missing classes. In the days
Question 2. You are seeing a 65-year old right-handed patient that followed, the boy became quite lazy and lost his sense of
who is complaining of weakness on the left side of his body. direction as described by his siblings. His grades in math have
On neurologic examination, you were able to elicit right-sided also surprisingly declined. The boy’s lesion can most likely be
facial weakness upon cranial nerve testing in addition to 2/5 localized to which lobe?
strength on the left upper and left lower extremities. Without A. Right Parietal
the aid of imaging studies, the lesion is likely localized to __? B. Left Parietal
A. Cerebral Cortex C. Right Frontal
B. Subcortex D. Left Frontal
Answer: B. This is a case of Gerstmann Syndrome, which usually occurs in clinical situation such as the one
C. Brainstem above. Recall that this syndrome is found if the dominant parietal lobe is damaged, whereby in 95% of the
population it is found in the left parietal cortex.
D. Spinal Cord
Answer: C. This is a lesion located in the brainstem due to the presentation of crossed symptoms.
Question 9. Aside from the above symptoms (refer to
Question 3. A stray bullet hits an innocent by-stander on her Question 8) described, which of the following is another
back, resulting in paralysis of the bilateral lower extremities. prominent symptom of this syndrome?
This is correctly termed as ____ and indicates a lesion in the A. Finger anosognosia
____? B. Simultagnosia
A. Paraplegia, Thoracic Spinal Cord C. Agraphesthesia
B. Paraparesis, Thoracic Spinal Cord D. Acalculia
Answer: D. Note that the tetrad of symptoms for Gertsmann Syndrome includes finger agnosia, right-left
C. Paraplegia, Cervical Spinal Cord disorientation, agraphia and acalcuiia. Simultagnosia is usually found in Balint’s Syndrome.

D. Paraparesis, Cervical Spinal Cord

Answer: A. Note that –plegia is paralysis while –paresis is weakness. Paraplegia Is weakness of the bilateral Question 10. A 59-year old woman who presented to the
lower extremities while quadriplegia is weakness of all extremities usually seen in cervical spinal cord lesions.
emergency room at a tertiary care center with a 3-day history
Question 4. The dorsal column medial lemniscal pathway of mental status changes. According to her accompanying
decussates at the level of the _____ located in the _____? spouse, 3 days prior, she had eaten out and had one episode
A. Medial Lemniscus, Upper Medulla of diarrhea. Since then, she had slowly become increasingly
B. Mediolateral Lemniscus, Upper Medulla confused, trouble finding the right words and has been using
C. Medial Lemniscus, Lower Medulla incorrect words in sentences. These were accompanied by
D. Mediolateral Lemniscus, Lower Medulla mild anorexia and frontal headache. Neurologic examination
Answer: A. There is no such thing as the mediolateral lemniscus. The corticospinal tracts decussate at the level of shows mild dysnomia and subsequent cranial MRI showed
the lower medulla, not the DCML.
lesions, which would most likely be localized to which lobe?
Question 5. You are seeing a 55-year old patient with multiple A. Frontal Lobe
hypopigemented patches distributed in the trunk and B. Parietal Lobe
extremities. There is associated loss of sensation but no C. Temporal Lobe
pruritus. On further history taking, you note that the patient has D. Occipital Lobe
lives in the tropics for decades. Your top differential diagnosis Answer: C. This is a case Herpes Simplex encephalitis, which most commonly affects the temporal lobe as
manifested by Wernicke’s aphasia present in the patient, which is located in the left superior temporal lobe.
for the patient’s case includes infection caused by ___?
A. Nematodes Question 11. Confusion, trouble finding the right words and
B. Virus use of incorrect words as seen in our patient (refer to question
C. Protozoa 10) is correctly termed as what type of neurologic deficit?
D. Bacteria A. Expressive Aphasia
Answer D. This is a classic case of tuberculoid leprosy. Viruses that can cause neurologic symptoms include B. Reciprocal Aphasia
herpes simplex virus, varicella, and rabies virus. Protozoa such as Naegleria and Acanthamoeba cause
meningoencephalitis. Nematodes are not known to cause neurologic symptoms. C. Fluent Aphasia
D. Non-fluent Aphasia
Question 6. A 30-year old patient comes to your clinic and is Answer: C. Remember Wernicke’s = fluent = receptive aphasia while Broca’s = non-fluent = expressive aphasia.
accompanied by a companion who states that he has seen the
patient sucking his thumb uncontrollably. On neurologic Question 12. Should our patient (refer to question 10) have a
examination, (+) grasp reflex is elicited. Where is the most severe lesion in the affected lobe, this would result in what
likely location of your patient’s lesion? characteristic visual field deficit?
A. Parietal Lobe A. Superior Quadrantonopsia
B. Frontal Lobe B. Inferior Quadrantanopsia
C. Temporal Lobe C. Bitemporal Hemianopsia
D. Occipital Lobe D. Homonymous Hemianopsia
Answer: B. This is because the inferior loop of the optic radiations course through the temporal lobe. A lesion in
Answer: B. Thumb sucking and (+) grasp reflexes are primitive reflexes normally seen in newborns. Maturation of the parietal lobe would manifest with superior quadrantonopsia since the superior loop of the optic radiations
the prefrontal cortex results in inhibition of these primitive reflexes/frontal release signs. course through the parietal lobe.
Question 13. Occipital lobe lesions do not usually cause Question 19. While doing your neurologic examination of a
affectation of macula, unless the lesion results in an occlusion patient, you ask her to put his arms on the side while standing
to the supply of the macula at the level of which important upright and thereafter closing his eyes. You notice swaying
blood vessel? enough to cause the patient fall on his right side. You ask the
A. External Carotid Artery patient to open his eyes, causing minimal swaying and thereby
B. Internal Carotid Artery prevented him from falling on his right side. The lesion of this
C. Middle Cerebral Artery patient is most likely localized to which system?
D. Posterior Cerebral Artery A. Dorsal Column Medial Lemniscal System
E. Both C and D are correct. B. Cerebellum
Answer: B. Lesions at the level of Internal Carotid Artery are sufficient to cause macular affectation since this is
enough to cause ischemia of the macula. C. Vestibular System
D. Anterolateral System
Question 14. The lower part of the face receives ___ Answer: C. This is Romberg’s Test, and with correction or prevention of fall upon opening of the eyes indicates
the correction by the eyes is sufficient to compensate for a dysfunctional vestibular system.
innervation from the motor cortex while the upper part of the
face receives _____ cortex. _____ lesions of CN VII result in Question 20. M.P. is a 50-year old patient who presented with
central facial palsy while ____ lesions of CN VII result in gradual onset of tremors, difficulty in initiating movement and
peripheral facial palsy. robot-like gait that started around 1 year PTC, which he
A. Unilateral, Bilateral; Supranuclear, Infranuclear ignored as simply normal signs of aging. He was previously a
B. Unilateral, Bilateral; Infranuclear, Supranuclear world-renowned boxing champion, but retired at the age of 40
C. Bilateral, Unilateral; Supranuclear, Infranuclear after consecutive losses. The lesion of M.P is localized to
D. Bilateral, Unilateral; Infranuclear, Supranuclear ____, which secretes dopamine, normally causing _____?
Answer: A. Recall very well the difference between central and peripheral facial palsy. Central = from the UMN,
Peripheral = from the LMN.
A. Basal Ganglia, stimulation of movement
B. Substantia Nigra Pars Compacta, stimulation of movement
Question 15. A 55-year old woman from Pampanga presents C. Substantia Nigra Para Reticularis, stimulation of movement
with a 1-month history of inward deviation of the eyeball. There D. Caudate Nucleus, inhibition of movement
is associated deafness, tinnitus, epistaxis and cervical Answer: B. This is a case of early-onset Parkinson’s Disease, termed as Dementia Frugilistica, caused by
repeated head trauma common in boxers.
lymphadenopathy. Given the inward deviation of the eyeball,
which cranial nerve is most likely affected? Question 21. A 60-year old widow presented with a 1-month
A. CN II onset of “slowness” and “lack of focus”. The children of the
B. CN III patient claims that the patient seems uninterested in daily living
C. CN IV and claims that the patient would rather sleep for the whole day
D. CN VI than spend time with them. Upon doing your MMSE testing, it
Answer: D. As you will learn later on, this is a case of nasopharyngeal carcinoma causing a specific CN VI palsy
due to affectation of the pathway of the abducents nerve. Inward deviation of the eyeballs means there is an
shows intact attention and concentration despite the patient
overfunctioning medial rectus and loss of function of the lateral rectus, which is innervated by CN VI. Remember
LRA, SOT as mnemonic for EOMs.
initially insisting that he does not know the answers to the
questions. Which of the following statements about the patient
Question 16. A 25-year old man was shot at his back while is TRUE?
being chased down the police. Upon consult at the ER, he A. The patient has dementia, and the MMSE was not done
presented with the weakness of his left leg, loss of vibration correctly. MMSE needs to be repeatedly done.
and position sense of his left leg, and loss of pain and B. The patient has dementia, and the MMSE was done
temperature sensation of his right leg. All of the following correctly. Start the patient on physical and occupational
systems are affected, EXCEPT? therapy programs.
A. Dorsal Column Medial Lemniscal System C. The patient does not have dementia, and the MMSE is
B. Anterolateral System expected to be normal.
C. Corticorubral Tract D. The patient does not have dementia, and the MMSE is
D. Corticospinal Tract expected be abnormal.
Answer: C. This is a classic case of Brown Sequard Syndrome, caused by hemitransection of the spinal cord. A Answer: C. This is a case of pseudodemntia, where predominantly depressive symptoms appear to cause mental
bullet hit this patient causing a left hemitransection of the thoracic spinal cord, causing ipsilateral weakness and slowness and lack of ability to focus and concentrate. This can be differentiated from true dementia by the MMSE,
loss of position and vibration sense since CST and DCML have not yet decussated while causing contralateral where demented patients would give wrong answers, have poor attention and concentration, and appear
contralateral loss of pain and temperature sense since ALS decussates immediately upon entry into the spinal indifferent/unconcerned.
cord.

Question 22. An aneurysm of the posterior cerebral artery

Question 17. A 62-year old woman came into the ER due to
commonly results in affectation of which cranial nerve?
sudden onset of right-sided weakness and left-sided “down”
A. CN II
and “out” eyeball associated with miosis and mydriasis. The
B. CN III
lesion of this woman is most likely localized to which area?
C. CN IV
A. Right Subcortex
D. CN VI
B. Left Internal Capsule Answer: B. CN III is located in the area adjacent to the posterior cerebral artery, thereby aneurysms causing
C. Left Midbrain compression of CN III cause ptosis, mydriasis and a characteristic “down and out” eyeball.

D. Left Pons Question 23. The correct description for dysesthesia:

Answer: C. This is a case of Weber Syndrome, which is caused by occlusion of posterior cerebral artery that
supplies the medial superior midbrain area where the corticospinal tract (causing the contralateral weakness) and A. Spontaneous unpleasant, abnormal sensations which are
CN III (causing down and out due to overfunctioning lateral rectus and superior oblique) are located.
electrical in quality
Question 18. The motor homunculus that exist in the B. Noxious stimuli but exaggeratedly perceived as painful
cerebellum indicates that the trunk, head and neck area are C. Non-noxious stimuli but perceived as painful
represented by the ___ while the extremities are represented D. Provoked unpleasant, abnormal sensations which are
by the ___. electrical in quality
Answer: D. Remember that A is paresthesia, as one would experience after crossing his/her legs for long minutes
A. Vermis, Cerebellar Hemisphere and hours. B is allodynia (Remember A for Arte), and C is hyperpathia. Dysesthesia is same as paresthesia but is
B. Vermis, Anterior Lobe provoked.

C. Cerebellar Hemisphere, Vermis

D. Anterior Lobe, Vermis
Answer: A. The vermis located in the most medial part of the cerebellum is responsible for coordinating
movements in the axis of the body while cerebellar hemispheres are responsible for coordination of the
extremities.
Question 24. Which of the following is the correct description Question 29. A 22-year old patient comes in for complaints of
for a post-stroke patient, who on manual muscle testing, high-grade fever, headache and difficulty sleeping for around 5
showed active movement against gravity but upon application days. Upon neurologic examination, you are able to elicit
of some resistance, the patient can no longer actively move the positive meningeal signs. Which of the following is the BEST
extremity being tested? step in diagnosing this patient’s disease?
A. 1 A. Complete Blood Count
B. 2 B. Lumbar Puncture and CSF Analysis
C. 3 C. Cranial MRI with Contrast Enhancement
D. 4 D. Toxicology Screen
Answer: C. Remember and master the muscle strength grading. 1 is a barely detectable trace of contraction, 2 is Answer: B. The patient is presenting with classic signs and symptoms of meningitis. Lumbar puncture with CSF
active movement of the body with gravity eliminated, and 4 is active movement against gravity and some analysis is the best diagnostic method to confirm meningitis and differentiate its specific type. Complete blood
resistance. count can aid in confirming an infection. Imaging studies such as cranial MRI can aid in assessing the extent of
the disease, which would normally show meningeal thickening. Toxicology screening is not usually indicated for
meningitis.
Question 25. Upon eliciting the patient’s reflexes, you obtain
the following results: Biceps reflex +, Triceps Reflex ++, Question 30. While doing your neurologic examination of a
Brachioradialis +, Patellar Reflex ++, Achilles Reflex ++. With patient, you ask her to put her arms on the side while standing
these results, we can localize the specific LMN lesion of our upright and thereafter closing her eyes. You notice swaying
patient in which nerve roots? enough to cause the patient fall on her left side. You ask the
A. C4, C5 patient to open her eyes, but the swaying persisted and the
B. C5, C6 patient still fell on her left side. The lesion of this patient is most
C. C6, C7 likely localized to which system?
D. C7, C8 A. Dorsal Column Medial Lemniscal System
Answer: C. Remember the specific roots corresponding to each reflex: C5-C6 for biceps and brachioradialis, C6-
C7 for triceps, L2-L3-L4 for patellar, and S1 for Achilles. B. Cerebellum
C. Vestibular System
Question 26. You are suspecting patient with an UMN lesion D. Anterolateral System
and upon neurologic examination, you are tasked to elicit the Answer: B. This is Romberg’s Test, and without correction or prevention of fall upon opening of the eyes indicates
the correction by the eyes is insufficient to compensate from a damaged cerebellum.
Babinski reflex. This reflex is correctly elicited by doing the
following: Question 31. A 40-year old woman presents with acute onset
A. Lateral side of the sole of the foot is rubbed with a blunt of inability to speak, left facial drooping, left arm and leg
instrument that runs from the heel along a curve to the toes. weakness, and right gaze preference. Where is this lesion
B. Medial side of the sole of the foot is rubbed with a blunt most likely localized?
instrument that runs from the heel along a curve to the toes. A. Cortex
C. Lateral side of the sole of the foot is rubbed with a blunt B. Subcortex
instrument that runs from the toes along a curve to the heel. C. Brainstem
D. Medial side of the sole of the foot is rubbed with a blunt D. Spinal Cord
instrument that runs from the toes along a curve to the heel. Answer: A. Apply the steps in neurolocalizaton. Using these steps, we can localize the lesion to the cortex since
there is abnormal cortical function due to inability to speak or Broca’s aphasia. This is likely an MCA stroke
Answer: A. Remember that this is correct method to elicit the Babinski reflex. Never use a sharp instrument as caused by occlusion of the superior division of the MCA, causing ischemia/infarction the right frontal lobe.
this can harm the patient.

Question 27. You are presented with a 30-year old male Question 32. A 40-year old patient comes in with acute onset
patient who presents with frequent falls on the right side of his of right-sided weakness. On neurologic examination, you were
body. Upon neurologic examination, you elicit that he has able to elicit 1/5 strength on the right side of face, right arm and
dysmetria and intention tremor on the right side, explaining his right leg, in addition to numbness of the entire right side and
tendency to fall on that side. Which of the following is the best (+) Babinski reflex.
method to test for a cerebellar lesion? A. Cortex
A. Finger to Nose Test B. Subcortex
B. Romberg’s Sign C. Brainstem
C. Tandem Gait D. Spinal Cord
Answer: B. Apply the steps in neurolocalizaton. Using these steps, we can localize the lesion to the subcortex due
D. Rapid Alternating Movements to equal affectation of the face, arm and legs.
Answer: A. The finger-to-nose test is the best test to test for a cerebellar lesion. Remember that a right-sided
dysmetria and intention tremor most likely indicates a right-sided cerebellar lesion. Romberg’s sign indicates a
multisensory deficit. Tandem gait tests mainly the motor system and cerebellar system. Rapid Alternating
Question 33. Patient W.S. is a 50-year old patient who came
Movements is used to elicit dysdiachokinesia. in due to right-sided numbness, tendency to fall on the left side
and left-sided facial numbness associated with dysarthria,
Question 28. A patient comes to your clinic due to complaints
dysphonia and vertigo. Without doing your neurologic
of weakness of his lower extremities. On neurologic
examination, where can this lesion be localized?
examination, you observe that he needs to lift his legs higher
than normal to be able to walk properly. This characteristic gait A. Cortex
is called ___ and is caused by foot drop due to loss of ___? B. Subcortex
C. Brainstem
A. Steppage Gait, Plantarflexion
D. Cerebellum
B. Waddling Gait, Knee Flexion Answer: C. Apply the steps in neurolocalizaton. Using these steps, we can localize the lesion to the brainstem due
C. Waddling Gait, Knee Extension to the crossed deficits, specifically in the medulla, a syndrome called Wallenberg Syndrome secondary to
occulusion of the posterior inferior cerebellar artery.
D. Steppage Gait, Dorsiflexion
Answer: D. The steppage gait is characterized by loss of dorsiflexion, and along with waddling gait, maybe one of
the earliest clinical signs of a motor neuron disease, such as ALS.
Question 34. Cerebellar lesions usually manifest with all of the
following symptoms, EXCEPT?
A. Decreased muscle tone
B. Nystagmus
C. Action tremor
D. Hemiparesis
Answer: D. Remember the mnemonic HANDST, which stands for hypotonia, asynergy of antagonist muscles,
nystagmus, dysmetria/dysarthria, stance and gait problems, and tremors (action/intention > resting).
Question 35. A 37-year old patient comes to your clinic for Question 41. A 40-year old male patient comes in complaining
long-standing shooting pain that radiates down his right leg. of weakness of right arm weakness followed by right leg
There is associated weakness of the bilateral extremities, weakness, left leg weakness and left arm weakness. There is
rendering him unable to stand and walk properly without now noted difficulty in swallowing. On neurologic examination,
assistance. Where can this lesion be localized? he has a hyporeflexic biceps and triceps reflex, and
A. Cortex hyperreflexic patellar and ankle reflexes, (+) Babinski sign.
B. Subcortex Where is the most likely location of the patient’s lesion?
C. Brainstem A. Motor Neuron
D. Spinal Cord B. Root
Answer: D. This is specifically a lesion probably in the lower thoracic to upper lumbar region of the spinal cord,
affecting nerve roots, hence causing the characteristic pain seen in radiculopathy. C. Peripheral Nerve
D. Nerve Plexus
Question 36. A 28-year old man is seen at the ER following a Answer: A. This is a case of motor neuron disease, commonly seen in ALS or Lou Gehrig’s Disease. Note the
hallmark of mixed upper and lower motor neuron signs, and also characteristic asymmetry on initial presentation
motorcycle crash accident occurring a few minutes PTC. You becoming symmetric when the disease becomes chronic in duration.

observe flexion of the upper extremities and extension of the

Question 42. A 45-year old patient comes to your clinic for
lower extremities. This is termed as ___ and indicates a lesion
long-standing shooting pain that radiates down his lower
___.
extremities. There is associated weakness and numbness of
A. Decorticate posturing, above the red nucleus
the bilateral extremities, rendering him unable to stand and
B. Decorticate posturing, below the red nucleus
walk properly. Where can this lesion be localized?
C. Decerebrate posturing, above the red nucleus
A. Root
D. Decerebrate posturing, below the red nucleus
Answer: A. Note that it is not strictly damage to the sparing of the red nucleus from the rubrospinal tract that B. Peripheral Nerve
results in this type of posturing since this results in flexion of the upper extermities predominantly. It also involves
the corticospinal tract subserving the flexors of the lower extremity, resulting in extension of the lower extremities.
C. Neuromuscular Junction
D. Muscle
Question 37. If the patient above (refer to Question 36) has Answer: A. Remember the hallmark of radiculopathy, which is PAIN. In addition, presence of numbness
automatically eliminated NMJ and muscle disorders as only root and peripheral nerve disorders present with
incomprehensible mumbles and eye opening only upon sensory loss.

application of pain stimuli, what is the GCS score of this

Question 43. A patient is found to have weakness of abduction
patient?
of the little finger on the right hand and reduced pain sensation
A. GCS 8 (E3 V2 M3)
on the palmar surface of the little finger of the right hand. This
B. GCS 7 (E2 V2 M3)
lesion is most likely localized to ___?
C. GCS 9 (E2 V2 M4)
A. Radial Nerve
D. GCS 6 (E2 V2 M2)
Answer: B. Master the component of the GCS. Remember that we must indicate the specific scores to each B. Ulnar Nerve
component rather than just the overall score. A GCS<8 indicates respiratory depression and this patient will likely
require intubation. C. Axillary Nerve
D. Median Nerve
Answer: B. This is a classic case of ulnar nerve mononeuropathy. Note that the ulnar nerve innervates the palmar
Question 38. A 40-year old female patient was seen at the ER and dorsal surface of the lateral 1/3 of the hand and innervates the abductor digiti minimi.

due to sudden onset of headache, vomiting, weakness of all

extremities and seizures. After a few minutes, the patient was Question 44. A 55-year old woman presents with eyelid
seen to have arms extended, wrists rotated, legs extended and drooping and diplopia. She complains that her arms become
feet internally rotated. This is termed as ___ and indicates a heavy when she crochets from long periods of time with relief
lesion ___ upon resting. There are no other associated symptoms. Where
can this lesion be localized?
A. Decorticate posturing, above the red nucleus
B. Decorticate posturing, below the red nucleus A. Root
C. Decerebrate posturing, above the red nucleus B. Peripheral Nerve
D. Decerebrate posturing, below the red nucleus C. Neuromuscular Junction
Answer: D. Note that removing the influence of the rubrospinal tract subserving flexion of the upper extremities D. Muscle
allows the other indirect activation pathways to dominate, resulting in extension of the arms, in addition to Answer: C. This is a classic case of ocular myasthenia gravis, with FATIGABILITY as the hallmark of NMJ
extension of the legs. disorders. Diagnostic maneuvers tests can include single breath counting test (abnormal if patient cannot count to
10 while holding his/her breath) and repetitive nerve stimulation.

Question 39. If the patient above (refer to Question 38) has no

verbal output and eye opening only upon application of pain Question 45. A 7-year old patient comes in to your clinic due
stimuli, what is the GCS score of this patient? to history of repeated falls, fatigue and inability to climb stairs
but with normal mentation and no other associated symptoms.
A. GCS 5 (E2 V1 M2)
This patient’s lesion is most likely localized to ___?
B. GCS 5 (E2 V0 M3)
C. GCS 4 (E2 V1 M1) A. Root
D. GCS 4 (E1 V1 M2) B. Peripheral Nerve
Answer: A. Master the component of the GCS. Remember that we must indicate the specific scores to each C. Neuromuscular Junction
component rather than just the overall score. A GCS<8 indicates respiratory depression and this patient will likely
require intubation. D. Muscle
Answer: D. Muscle. This is a case of Duchenne’s Muscular Dystrophy characterized by early-onset weakness of
the PROXIMAL than distal muscles hence causing inability to climb stairs (requires use of proximal thigh
Question 40. A 58-year old male patient comes with due to muscles). Examination can show pseudohypertrophy of the affected muscles, elevated creatine kinase levels and
(+) Gower’s Sign.
sudden onset weakness of the right arm and weakness in the
left lower extremity following trauma to the upper neck. What is Question 46. A 33-year old patient who works as an online
the explanation for this patient’s symptoms? transcriptionist is complaining of recurrent numbness and
A. There is a brainstem infarction resulting in crossed deficits. weakness of his hands. You tap the ventral surface of his wrist
B. The patient is lying because this pattern of weakness is not area and suddenly, the patient complains of “pins and needles”
possible theoretically and clinically. sensation. The sign you elicited is called ___?
C. There is a lesion in the area of decussation of the A. Phalen’s Sign
corticospinal tract secondary to trauma. B. Reverse Phalen’s Sign
D. There is a lesion in the area of decussation of the C. Prayer’s Sign
corticospinal tract secondary to infarction. D. Tinel’s Sign
Answer: C. This characteristic pattern of weakness is seen in selective injury to the superior cervical spinal cord Answer: D. Note that Phalen’s sign is elicited by asking the patient to hold out the arms, flexing the wrists and
secondary to trauma. This type of paralysis is known as CRUCIATE paralysis. letting the hands hang down. Reverse Phalen’s /Prayer’s sign is elicited by holding out the arms, extending the
wrist and hands hang up.
Question 47. A pregnant patient is now into the early third Question 53. A 55-year old patient presents with dizziness
trimester of her current pregnancy and comes to your clinic upon abrupt change in positions, with associated nausea and
complaining of numbness of the thighs. Which of the following vomiting during the episodes. She is currently on Betahistine
nerve is most likely affected? once daily to prevent or minimize the episodes of dizziness.
A. Anterior Femoral Cutaneous Nerve Which of the following is characteristic of this condition?
B. Lateral Femoral Cutaneous Nerve A. The attacks occur only occasionally.
C. Anterolateral Femoral Cutaneous Nerve B. There attacks are paroxysmal and each episode can last for
D. Common Peroneal Nerve more than 5 minutes.
Answer: C. This is a classic case of lateral femoral cutaneous nerve injury. Pregnancy increases abdominal girth
causing nerve compression of the nerve as it passes under the inguinal ligament. C. The attacks last only for seconds or less than a minute.
D. There is associated hearing loss on the affected side.
Question 48. A 21-year old male colleagiate wrestler presents Answer: C. BPPV is characterized by a paroxysmal vertigo and nystagmus especially on changes in position, with
attacks lasting LESS THAN A MINUTE or for only SECONDS, with no associated hearing loss. The attacks recur
to your clinic with left elbow pain, associated with decreased periodically for months to years.

sensation along the medial forearm and decreased motor

Question 54. A 58-year old patient comes in due to severe
function in his hands and wrist. The patient recalls partial loss
attacks of dizziness that last for days with associated nausea
of function following a direct below to the ___?
and vomiting, and tinnitus and deafness. The cause of the
A. Spiral Groove
patient’s vertigo is likely ___?
B. Cubital Tunnel
A. Peripheral
C. Guyon’s Canal
B. Central
D. Carpal Tunnel
Answer: B. This is a classic case of ulnar nerve neuropathy/cubital tunnel syndrome following direct trauma to the C. Insufficient information is given to conclude whether the
elbow, likely damaging the ulner nerve as it passes through the cubital tunnel.
lesion is peripheral or central in origin
Question 49. A 24-year old male patient was brought to the D. The presence of tinnitus and deafness makes a vestibular
ER after sustaining multiple physical injuries. Upon seeing the lesion unlikely.
Answer: A. Remember the table on differences between peripheral and central causes of vertigo. Nausea,
patient, you observe that he mostly responds with incoherent vomiting, tinnitus and deafness are characteristics of a peripheral cause of vertigo.

mumbles, doses off while responding to stimuli but still able to

Question 55. A 30-year old patient comes in due to deafness,
follow simple commands. How would you describe the patient’s
and prolonged balance problems. There is associated facial
level of consciousness?
asymmetry and ipsilateral ataxia. The cause of the patient’s
A. Lethargic
symptoms is likely ___?
B. Obtunded
A. Peripheral
C. Stuporous
B. Central
D. Comatose
Answer: A. Lethargy is characterized by the patient’ above plus disorganized movements. The important C. Insufficient information is given to conclude whether the
characteristic is still being able to follow simple commands, which if he is unable to do so, he would be classified
as obtunded.
lesion is peripheral or central in origin
D. The presence of deafness and balance problems makes a
Question 50. The same patient above (refer to Question 49) vestibular lesion unlikely.
was seen by the ER doctor on duty and saw that his pupils Answer: B. Remember the table on differences between peripheral and central causes of vertigo. While deafness
is a more commonly seen in peripheral causes of vertigo, the presence of focal neurologic deficits makes a
were pinpoint with barely perceptible reaction to strong light. central lesion more likely. Do an cranial MRI for this patient to rule out a cerebellopontine angle tumor.

Based on the pupillary reaction, the location of the lesion is

Question 56. The following somatosensory deficits are
most likely in the ___?
described as positive sensory deficits, EXCEPT?
A. Midbrain
A. Paresthesia
B. Pons
B. Dysesthesia
C. Diencpehalon
C. Allodynia
D. Non-localizable lesion. This is a metabolic encephalopathy.
Answer: B. Remember, pinpoint pupils = pontine lesion. D. Hypoesthesia
Answer: D. A, B and C are positive symptoms because they cause added sensations. Hypoesthesia causes
characteristic decreased sensation, which is negative symptom.
Question 51. You are seeing a patient with altered sensorium
and while eliciting the Doll’e eye reflex, you observe the Question 57. The correct definition for syncope is ___?
following: Head turn to the right is followed by eyes turning to A. Rapid onset of transient loss of consciousness with an
the left. Head turn to the left is followed by eyes turning to the inability to maintain postural tone followed by spontaneous
right. Head turned upwards is followed by eyes going down recovery
while head turned downward is followed by eyes going up. B. Rapid onset of permanent loss of consciousness with an
What can we infer from these results? inability to maintain postural tone followed by spontaneous
A. Brainstem is intact. recovery.
B. Midbrain lesion is likely. C. Rapid onset of transient loss of consciousness with an
C. Pontine lesion is likely. inability to maintain postural tone followed by delayed recovery.
D. Non-conclusive results D. Rapid onset of permanent loss of consciousness with an
Answer: A. The normally inhibited Doll’s eye reflex in conscious patients is lost when sensorium is altered,
especially in comatose patients. The results seen with the patient are typical for an intact Doll’s eye inability to maintain postural tone followed by delayed recovery.
reflex/oculocephalic reflex. Any deviation from this pattern indicates a brainstem lesion, where the CN subserving Answer: A. The closes differential diagnosis for syncope is seizures. Remember, it is RAPID ONSET,
the EOMs are located. TRANSIENT loss of consciousness, and SPONTANEOUS recovery.

Question 52. Which of the following is INCORRECT about the

Dix-Hallpike Test?
A. Patient is seated and turned to one side at 30 degrees.
B. Patient is then helped to recline rapidly so that the head
hangs over the table
C. Within several seconds, this test elicits vertigo and
nystagmus that is horizontal with a rotary component.
D. Frenzel goggles can be used to aid in observing for
nystagmus since this disables visual fixation that can suppress
nystagmus.
Answer: A. Other choices are correct. However, the head is turned to one side at 45 DEGREES, not 30 degrees.
This is used to align the posterior semicircular canal with the sagittal plane of the head.
Question 58. A 74-yeard old patient sought was brought to Question 62. A 28-year old female is referred to your clinic
consult at the ER after 2 episodes of fainting within 24 hours. because of odd behavior. She had an episode witnessed by
He has a past history of hypertension, dyslipidemia, diabetes her mother where she suddenly stood up, mumbled
mellitus, and previous CABG but no recurrent chest pains. He incoherently, and fell to the floor, had a few jerks, and with
was seen just sitting down while reading book during the noted urinary incontinence. She woke up a few minutes later
attacks. There was no nausea and vomiting, and diaphoresis. and could not recall what happened. Her neurologic
He appeared pale and was unconscious for about 1 minute examination is normal. Laboratory tests and imaging did not
with no movements of bowel/bladder dysfunction. He woke up reveal any abnormality. Based on the patient’s case above,
feeling normal. The rest of the history and physical examination what is the type of seizure?
were unremarkable. Based on the patient’s case, what is the A. Simple Partial
most likely diagnosis? B. Complex Partial
A. Cardiac Syncope – Electrical cause C. Secondarily Generalized
B. Cardiac Syncope – Structural cause D. Generalized
C. Orthostatic-mediated Syncope Answer: C. Note that the patient started with intact consciousness then subsequently collapsed and lost
consciousness, characteristic of secondarily generalized seizures
D. Vasovagal Syncope
Answer: A. The history is consistent with a cardiac syncope, specifically an electrical cause that can occur with Question 63. If the patient above (refer to Question 62) had
the patient at rest. If patient was seen doing exertion, this likely rules in a structural cause.
persistent odd behavior for an extended period of time, this
Question 59. Based on the patient’s case above (refer to would be termed as ___ and one consideration for this
Question 58), which of the following laboratory tests is condition is prolonged convulsive status for longer than ___?
absolutely critical for diagnosis of the patient’s cause of A. Status Epilepticus, 3 minutes
syncope? B. Status Epilepticus, 5 minutes
A. Complete Blood Count C. Status Epilepticus, 15 minutes
B. Stat EEG D. Status Epilepticus, 30 minutes
C. 12-L ECG Answer: B. The strict definition is 15-30 minutes. However, in the context of clinical practice, it is more practical to
consider 5 minutes as the threshold since this condition requires immediate treatment due to cardiorespiratory
D. 2D Echocardiography dysfunction, hyperthermia, metabolic derangements that can lead to irreversible neuronal injury.
Answer: C. Electrical causes point to rhythm abnormalities and a 12-L is absolutely critical for diagnosing the
specific type of dysrhythmia causing ineffective pumping action of the heart and subsequently causing decreased Question 64. Normal cerebral blood flow is ___ and critical
blood flow to the brain. If a structural cause is suspected, a 2D echocardiography can be done.
level of hypoperfusion that abolishes brain function leading to
Question 60. Based on the patient’s case above (refer to tissue damage is ___?
Question 58), what laboratory test can you request for to rule A. 50-55ml/100g brain tissue/minute, 10-12 ml/100g brain
out the closest differential diagnosis for the patient’s case? tissue/minute
A. Complete Blood Count B. 50-55ml/100g brain tissue/minute, 12-23 ml/100g brain
B. Stat EEG tissue/minute
C. 12-L ECG C. 60-65ml/100g brain tissue/minute, 10-12 ml/100g brain
D. 2D Echocardiography tissue/minute
Answer: B. Again, seizures are the closest differential diagnosis for syncope and EEG can be used to monitor for
possible subclinical or non-convulsive seizures D. 60-65ml/100g brain tissue/minute, 12-23 ml/100g brain
tissue/minute
Question 61. The correct definition for seizure is ___? Answer: B. These values are critical since anything less than the 12 ml/100g/minute can already lead to infarction.

A. Transient and irreversible alteration of behavior caused by a Question 65. The most common site for an intracerebral
paroxysmal, abnormal and excessive neuronal discharge from hemorrhage to occur is in the ___?
pathologically excitable neurons.
A. Putamen
B. Transient and reversible alteration of behavior caused by a
B. Subthalamic Nucleus
paroxysmal, abnormal and excessive neuronal discharge from
C. Internal Capsule
pathologically excitable neurons.
D. Cerebellum
C. Transient and irreversible alteration of behavior caused by a Answer: A.
occasional, abnormal and excessive neuronal discharge from
pathologically excitable neurons. Question 66. A 75-year old patient was brought to the ER after
D. Transient and reversible alteration of behavior caused by a sudden onset of right-sided weakness and numbness with
occasional, abnormal and excessive neuronal discharge from slurring of speech. He went to bed at 2300H and was seen with
pathologically excitable neurons. these symptoms at 0500H the following day. What is the time
Answer: B. This definition closely resembles that of syncope but there are indeed a few differences, especially in of ictus and time that thrombolytics can be given based on the
the pathophysiology of seizures
golden hour of stroke?
A. 2300H, thrombolytics must ideally be given at 0200H
Question 61. The correct definition for seizure is ___? B. 2300H, thrombolytics must ideally be given at 0330H
A. Transient and irreversible alteration of behavior caused by a C. 0500H, thrombolytics must ideally be given at 0800H
paroxysmal, abnormal and excessive neuronal discharge from D. 0500H, thrombolytics must ideally be given at 0930H
Answer: A. Note that the time of ictus is the time that the patient was last seen normal and not the time at which
pathologically excitable neurons. he/she woke up already manifesting with the aforementioned symptoms. Golden hour is ideally at 3 hours but it
B. Transient and reversible alteration of behavior caused by a can be stretched to 4.5 hours.

paroxysmal, abnormal and excessive neuronal discharge from Question 67. The patient above (refer to Question 68) has a
pathologically excitable neurons. stroke most probably localized to the MCA. What visual deficit
C. Transient and irreversible alteration of behavior caused by a can we expect from the patient given his other neurologic
occasional, abnormal and excessive neuronal discharge from symptoms?
pathologically excitable neurons. A. Inferior quadrantonopsia
D. Transient and reversible alteration of behavior caused by a B. Superior quadrantonopsia
occasional, abnormal and excessive neuronal discharge from C. Homonymous Hemianopsia
pathologically excitable neurons. D. Bitemporal Hemianopsia
Answer: B. This definition closely resembles that of syncope but there are indeed a few differences, especially in
Answer: A. Note and remember the visual pathway as it passes through the parietal lobe area, where the superior
the pathophysiology of seizures
loop of the optic radiations is located.
Question 68. The mnemonic “SNOOPS” can be used to
identify red flags for headache and the mnemonic covers all of
the following red flag symptoms, EXCEPT:
A. Fever and stiff neck
B. Sudden onset
C. Neurologic deficits
D. Recurrent but constant in intensity
Answer: D. recurrent but constant in intensity of headaches is not a red flag since this points towards a primary
benign etiology. However, if it is becoming more frequent and increasing in intensity, that is a red flag.

Question 69. The characteristics typical for migraine headache

include the ff:
A. Periodic, predominantly unilateral, often dull/aching in
quality
B. Periodic, predominantly unilateral, often dull/aching in
quality
C. Periodic, exclusively unilateral, often pulsatile/throbbing
headaches.
D. Periodic, predominantly unilateral, often pulsatile/throbbing
headaches
Answer: D. Note that it is indeed periodic and can be bilateral but predominantly unilateral, with a pulsatile and
throbbing quality of headaches.

Question 70. A 26-year old right-handed female presents to

the ER with acute onset of severe headache. She states that
on her way to work few hours PTC, she suddenly felt a severe
and sharp pain in her head followed by loss of consciousness.
There was associated nausea, vomiting and neck pain. Vital
signs are stable. Patient appears to be in discomfort with eyes
shut closed, and neurologic examination is unremarkable.
Based on the patient’s case above, what is the probable
diagnosis?
A. Complicated Migraine
B. Tension Headache
C. Brain Tumor
D. Subarachnoid Hemorrhage
Answer: D. Choice A would usually present with migraine associated with a transient neurologic deficit that
resolves within 72 hours. Choice B is usually associated with stress but the patient mentioned no stress at the
workplace. Choice C usually presents with a chronic and progressive headache that is increasing in intensity.