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Neurological System

Aim of a neurological history and examination: determine whether a neurological

lesion is local or diffuse; and, to determine the location of the neurological lesion,
based upon 4 areas:
(i) Peripheral nerves
(ii) Spinal Cord
(iii) Posterior Cranial fossa (i.e. brainstem and/or cerebellum)
(iv) Cerebrum (i.e. higher functioning centres)

Summary of the neurological system examination:

(i) History with specific symptoms
• Headache, Facial/Neck/Back pain, Dizziness/Vertigo, Hearing and Vision,
Motor, Sensation, Gait, Movement, Speech and Swallowing, Altered mental
(ii) Observation and Inspection
• Face, limbs, trunk, muscles, speech, eyes, etc.
(iii) Cranial Nerves (CNII-CNXII)
(iv) Upper Limb and Lower Limbs
• Tone, Power, Reflexes, Sensation (touch, pain and vibration),
Proprioception, RoM
(v) Cerebellar Function (Gait, Balance and Speech)
(vi) Autonomic Function and Disease
(vii)Mini-Mental Examination

Elicit a History from Patients

Headache, back or neck pain

• Methodology: SOHCRATES and Prior Experiences/New
• Tension Headache:
o Bilateral, sensation of tightness, no other symptoms
• Migraine:
o Unilateral headache, preceded by aura, photophobia
o Aura:

 Localising: e.g. audio or visual hallucination; loss of speech

and taste, etc.
 Non-Localising: e.g. general feeling of apprehension
• Cluster Headache:
o Pain over one eye, associated with lacrimation, rhinorrhoea & flushing
of the forehead
o Predominantly in males
• Cervical Spondylosis:
o Pain over occiput, neck stiffness
o Definition: degenerative OA of the joints between the spinal vertebrae
or neural foramina
• Raised ICP:
o Generalised, worse in morning, drowsiness, vomiting/nausea
o Worse in morning due to less dehydration
• Meningitis:
o Generalised, photophobia, fever, neck stiffness
• Temporal Arteritis:
o Unilateral, tenderness over temporal artery, blurred vision
• Acute sinusitis:
o Pain behind eyes, forehead or cheeks
• Subarachnoid Haemorrhage:
o Severe headache, instantaneous

Facial pain
• Trigeminal neuralgia
o Neuropathic disorder of one or both CNV
o Extremely painful; nicknamed “suicide disease”
o Incidence: highest in >40y.o. and in women
o Pain associated with the mildest touch or no stimulation at al
o Pathology: possibly associated with compression of the trigeminal
nerve within the cranial cavity; i.e. by the superior cerebellar artery
• Temporomandibular arthritis
• Glaucoma (usually only in acute-angle glaucoma [genetic mutation, acute
o Optic neuropathy; leading to progressive, irreversible loss of vision
o Pathology: chronic elevation of intra-occular pressure; mechanism or
neuron injury not completely understood
o Incidence: leading cause of blindness in African Americans
o Painless, and often late diagnosis due to the preservation of foveal
vision until the late stages of disease
o Screening via measuring of intraocular pressure and cup:disc ratio
• Cluster headache
o Affects 0.1% of the population
o Men > women
o Nickname: “Suicide headache”
o >1year in duration, paroxysmal

• Temporal arteritis
• Psychiatric disease
• Aneurysm of internal carotid or posterior communicating artery
• Superior orbital fissure syndrome

Fits, faints or “funny turns”

• Epilepsy vs. syncope
• Epilepsy:
o Grand Mal Epilepsy: tonic-clonic seizures with loss of consciousness
and generally preceded by an aura; often incontinent and tongue
o Complex seizures: loss of consciousness
o Simple Seizures: uninhibited consciousness
o Petit Mal Epilepsy: occurs in children, and is characterised by loss of
awareness and staring into space; motor function un-involved
o Generalised vs. Localised (i.e. specific or non-specific components of
the seizure)
• Syncope:
o Cardiogenic
o Non-Cardiogenic

• TIA:
o Sometimes occur without necessary LOC
o Called “drop attacks”
• Hypoglycaemia (sweating, weakness, confusion)

Dizziness or vertigo
• Vertigo (true):
o There is actually a sense of motion, usually of the surroundings but
also of the head itself
o Symptoms (severe): nausea, vomiting, pallor, headaches, sweating
• Balance disorders
o Central: involving the CNS; include:
 TIA’s – most common cause of vertigo in people >40y.o.
 Common clinical signs:
• Bilateral nystagmus
 Symptoms more pronounced
o Peripheral: nerve, muscle, or end-organ; include:
 Meniere’s Disease
 Vestibular neuronitis (commonest cause of vertigo in people
 Acute labyrinthitis
 Ototoxic drugs (e.g. aminoglycoside’s associated with
deafness or tinnitus too)
 Acoustic neuroma (benign tumour growth on CNVIII)
 Internal auditory artery occlusion

Disturbances of vision, hearing or smell

• Vision:
o Diplopia = double vision
o Amblyopia = blurry vision
o Photophobia = light intolerance
• Hearing: causes of deafness include:
o Trauma: chronic, e.g. excess volume, iPods; acute, e.g. fracture of
petrous bone
o Tumours: acoustic neuroma
o Vascular: disease of the internal auditory artery, rare.

Classification of Gait Disorders:
1.Hemiplegia: the foot is plantar flexed and the leg is swung in a lateral arc
2.Spastic paraparesis: scissors gait
3.Parkinson's disease: hesitation in starting
• shuffling
• freezing
• festination
• propulsion

• retropulsion
4.Cerebellar: a drunken gait which is wide-based or reeling on a narrow
base; the patient staggers towards the affected side if there is a unilateral
cerebellar hemisphere lesion
5.Posterior column lesion: clumsy slapping down of the feet on a broad
6.Footdrop: high stepping gait
7.Proximal myopathy: waddling gait
8.Prefrontal lobe (apraxic): feet appear glued to floor when erect, but move
more easily when the patient is supine
9.Hysterical: characterised by a bizarre, inconsistent gait

Loss of Sensation or Motor function in upper and lower limbs

• Aim: to determine the location of the lesion
o UMN Lesions (Pyramidal weakness, greatest effect on anti-gravity
• Due to: interruption of a neural pathway at a level above the
anterior horn cell.
• Result: INCREASE tone and reflexes; DECREASE power
• There is little or no muscle wasting.
o LMN lesions:
• Due to: lesion that interrupts the reflex arc between the
anterior horn cell and the muscle.
• Result: DECREASE tone and reflexes, DECREASE power

• Fasciculation (irregular contractions of small areas of muscle)

may be seen
• Muscle wasting is prominent.
o Myasthenia Gravis:

• Autoimmune disease with antibodies specific for Ach receptors

at the post-synaptic junction
• Leads to fluctuating muscle weakness and fatigue
• DECREASED power (mainly repetitive movements); NORMAL
tone and reflexes
o Muscle disease causes weakness in a particular muscle or group of
o There is muscle wasting
(4) OTHER:
o e.g. hysteria
o Causes a non-anatomical pattern of weakness
o NORMAL tone and power; unless there has been prolonged disuse,
normal muscle bulk
o Nerve Entrapment/Peripheral Neuropathy:

• Pins and needles in hands & feet

o Carpal Tunnel Syndrome:

• Pain and parasthesia in hand and wrist

Disturbances of sphincter control

• Seizure
• Spinal cord tumour/trauma

Involuntary movements or tremor

• Parkinsons disease = resting tremor
• Cerebellar disease = intention tremor

Akithesia Motor restlessness; constant semi-purposeful movements of

the arms and legs
Asterixis Sudden loss of muscle tone during sustained contraction of
an outstretched limb
Athetosis Writhing, slow sinuous movements, especially of the hands
and wrists
Chorea Jerky small rapid movements, often disguised by the patient
with a purposeful final movement: e.g. the jerky upward arm
movement is transformed into a voluntary movement to
scratch the head
Dyskinesia Purposeless and continuous movements, often of the face
and mouth; often a result of treatment with major
tranquillizers for psychotic illness
Dystonia Sustained contractions of groups of agonist and antagonist
muscles, usually in flexion or extremes of extension; it results
in bizarre postures
Hemiballismus An exaggerated form of chorea involving one side of the
body: there are wild flinging movements which can injure the
patient (or bystanders)
Myoclonic jerk A brief muscle contraction which causes a sudden
purposeless jerking of a limb
Myokymia A repeated contraction of a small muscle group; often
involves the orbicularis oculi muscles
Tic A repetitive irresistible movement which is purposeful or
Tremor A rhythmical alternating movement

Speech and swallowing disturbance

• Dysarthria
o Difficulty with articulation
• Dysphonia
o Altered quality of the voice with reduction in volume
o Due to vocal cord disease
• Dysphasia
o Dominant higher centre disorder in the use of symbols for
o Receptive (Wernicke’s) - difficulty in comprehension
o Expressive (Broca’s) - difficulty in putting words together to make
meaning, nominal

Altered cognition

Past Medical History

• meningitis or encephalitis
• head or spinal injuries
• epilepsy or convulsions
• previous operations
• sexually transmitted disease (e.g. risk factors for HIV infection or syphilis)
• Medications (anticonvulsants, contraceptive pill, antihypertensive agents,
steroids, anticoagulants)
• Cardiovascular disease (CAD, peripheral vascular disease, AF)

Social History
• Smoking
• Occupation
• Exposure to toxins
• Alcohol

Family History
• Neurological disease
• Mental health

Risk Factors for cerebrovascular disease

• Hypertension
• Smoking
• Diabetes mellitus
• Hyperlipidaemia
• AF, bacterial endocarditis, MI
• Haematological disease
• Family history of stroke

Conduct a systematic physical examination on a patient

1. General observation
2. Cranial Nerve Examination
3. Upper and Lower Limb examination
4. Cerebellar Examination
5. Mini mental state examination

General Observation
• Consciousness
• Neck Stiffness
o Meningism (Kernig's signe should also be elicited if meningitis is
suspected. Flex each hip in turn, then attempt to straighten the knee
while keeping the hip flexed. This is greatly limited by spasm of the
hamstrings (which in turn causes pain) when there is meningism due
to an inflammatory exudate around the lumbar spinal roots.)
o Parkinson’s = resting tremor
o Cervical spondylitis
o Raised intracranial pressure
o Cervical fusion

Higher Centres and Speech

• Handedness (assess likely dominant hemisphere)
• Orientation (ask patient name, present location and date)
o Dementia
o Delerium
• Speech
o Ask patient to describe the room (promote flowing speech)
o Test comprehension (eg. Touch your chin, then your nose)
o Test repetition (eg. Repeat the phrase “no ifs and or buts”)
o Ask patient to name two objects you point at

Recognise (through conversation rather than formal assessment) and explain

speech abnormalities


• 1 Receptive (posterior) dysphasia. This is where the patient cannot

understand the spoken (auditory dysphasia) or written word (alexia). This
condition is suggested when the patient is unable to understand any
commands or questions or to recognise written words in the absence of
deafness or blindness. Speech is fluent but disorganised. It occurs with a
lesion (infarction, haemorrhage or space-occupying tumour) in the dominant
hemisphere in the posterior part of the first temporal gyrus (Wernicke's areaf).
• 2 Expressive (anterior) dysphasia. This is present when the patient
understands, but cannot answer appropriately. Speech is non-fluent. This
occurs with a lesion in the posterior part of the dominant third frontal gyrus
(Broca's areag). Certain types of speech may be retained by these patients.
These include automatic speech. The patient may be able to recite word
series such as the days of the week or letters of the alphabet. Sometimes
emotional speech may be preserved so that when frustrated or upset the
patient may be able to swear fluently. In the same way the patient may be
able to sing familiar songs while unable to speak the words. It is important to
remember that unless the lesion responsible for these defects is very large
there may be no reduction in the patient's higher intellectual functions,
memory or judgment. Some of these patients may incorrectly be considered
psychotic, because of their disorganised speech.
• 3 Nominal dysphasia. All types of dysphasia cause difficulty naming objects.
There is also a specific type of nominal dysphasia. Here objects cannot be
named (e.g. the nib of a pen) but other aspects of speech are normal. The
patient may use long sentences to overcome failure to find the correct word
(circumlocution). It occurs with a lesion of the dominant posterior
temporoparietal area. Other causes include encephalopathy or the
intracranial pressure effects of a distinct space-occupying lesion; it may also
occur in the recovery phase from any dysphasia. Its localising value is
therefore doubtful.
• 4 Conductive dysphasia. Here patients repeat statements and name objects
poorly, but can follow commands. This is thought to be caused by a lesion of
the arcuate fasciculus and/or other fibres linking Wernicke's and Broca's


• Here there is no disorder of the content of speech but a difficulty with

articulation. It can occur because of abnormalities at a number of levels.
Upper motor neurone lesions of the cranial nerves, extrapyramidal conditions
(e.g. Parkinson's disease) and cerebellar lesions cause disturbances to the
rhythm of speech.


• This is alteration of the sound of the voice, such as huskiness of the voice
with decreased volume. It may be due to laryngeal disease (e.g. following a
viral infection or a tumour of the vocal cord), or to recurrent laryngeal nerve

Cranial Nerve Examination

Cranial Nerve I: Olfactory Nerve (not tested routinely)

• Anatomy
o Purely sensory nerve. Fibres arise in mucous membrance of nose &
pass through cribriform plate of ethmoid bone to synapse in olfactory
bulb. Olfactory tract runs under frontal lobe & terminates in medial
temporal lobe on the same side
• Examination
o External appearance of nose (deformity, rash)
o Nasal vestibule
• Testing
o Test each nostril separately with a series of bottles containing familiar
smells (coffee, peppermint, vanilla)
• Causes of anosmia
o URTI, smoking, old age, ethmoid tumours, skull fracture, congenital,
meningioma of olfactory groove, post-meningitis

Cranial Nerve II: Optic Nerve

• Anatomy
o The optic nerve is not really a nerve but an extension of fibres of the
central nervous system that unites the retinas with the brain. It is
purely sensory, contains about a million fibres and extends for about 5
cm passing through the optic foramen close to the ophthalmic artery
and joining the nerve from the other side at the base of the brain to
form the optic chiasm. The spatial orientation of fibres from different
parts of the fundus is preserved so that fibres from the lower part of
the retina are found in the inferior part of the chiasm and vice versa.
Fibres from the temporal visual fields (the nasal halves of the retinas)
cross in the chiasm, whereas those from the nasal visual fields do not.
Fibres for the light reflex from the optic chiasm finish in the superior
colliculus, whence connections occur with both third nerve nuclei. The
remainder of the fibres leaving the chiasm are concerned with vision,
and travel in the optic tract to the lateral geniculate body. From here
the fibres form the optic radiation and pass through the posterior part
of the internal capsule, finishing in the visual cortex of the occipital
lobe. In their course they splay out so that fibres serving the lower
quadrants course through the parietal lobe, while those for the upper
quadrants traverse the temporal lobe. The result of the decussation of
fibres in the optic chiasm is that fibres from the left visual field
terminate in the right occipital lobe and vice versa.
• History
o Reduction in visual acuity
o Sudden loss of vision in one eye: embolus to retina, migraine,
temporal arteritis, optic neuritis, non-arteitic ischaemic optic
o Sudden loss of bilateral vision: bilateral occipital lobe infarction or
trauma, bilateral optic nerve damage, psychotic states, methyl alcohol
o Gradual loss of vision: cataracts, old age, acute glaucoma; macular
degeneration; diabetic retinopathy (vitreous haemorrhages); bilateral
optic nerve or chiasmal compression; and bilateral optic nerve
damage-for example, tobacco amblyopia
• Examination
o Visual acuity: wearing spectacles (if needed). Use a hand held eye
chart or wall chart. Test each eye separately
o Visual fields: Hold hat pin or pen at arms length. Tell patient to look
directly into your eyes. Test when pin can be seen in peripheral vision.
Pin should be brought into visual field from four main directions & four
diagonals, directly into centre of field of vision
 Concentric diminution of the field (tunnel vision) may be
caused by glaucoma; retinal abnormalities such as
chorioretinitis or retinitis pigmentosa; papilloedema; or acute
ischaemia, as with migraine. Normally even a reduced field of
vision widens as objects are moved further away. Tubular
diminution of the visual fields suggests hysteria. There is
always a small area close to the centre of the visual fields
where there is no vision (the blind spot). This is the area where
the optic disc is seen on fundoscopy and is the point where the
optic nerve joins the retina. The blind spot enlarges with
 Central scotomata, or loss of central (macular) vision, may be
due to demyelination of the optic nerve (multiple sclerosis
causes unilateral or asymmetrical bilateral scotomata); toxic
causes, such as methyl alcohol (symmetrical bilateral
scotomata); nutritional causes, such as tobacco or alcohol
amblyopia (symmetrical central or centrocecal scotomata);
vascular lesions (unilateral); and gliomas of the optic nerve
 Total unilateral visual loss is due to a lesion of the optic nerve
or to unilateral eye disease.
 Bitemporal hemianopia is due to a lesion that affects the centre
of the optic chiasm, damaging fibres from the nasal halves of
the retinas as they decussate. This will result in loss of both
temporal halves of the visual fields. Causes include a pituitary
tumour, a craniopharyngioma and a suprasellar meningioma.
 Binasal hemianopia is very rare and is due to bilateral lesions
affecting the uncrossed optic fibres, such as atheroma of the
internal carotid siphon
 Homonymous hemianopia is due to a lesion that damages the
optic tract or radiation, affecting the visual field on the right or
left side. For example, left temporal and right nasal field loss
will occur with a right-sided lesion. The exact nature of the
defect depends on the site of interruption of the fibres. In the
optic tract the defect is usually complete-there is no macular
sparing. In the more posterior optic radiation the macular vision
is usually spared if the cause is ischaemia, but not if a
destructive process such as tumour or haemorrhage is
responsible. The macular cortical area is thought to have some
additional blood supply from the anterior and middle cerebral
 Homonymous quadrantanopia is loss of the upper or lower
homonymous quadrants of the visual fields. This may be due
to temporal lobe lesions (e.g. vascular lesions or tumours),
which cause upper quadrantanopia, or parietal lobe lesions
(e.g. vascular lesions or tumours), which cause lower
o Pupillary Reflexes: Using a pocket torch, shine the light from the side
into one of the pupils to assess its reaction to light. Inspect both pupils
and repeat this procedure on the other side.
 Normally the pupil into which the light is shone constricts
briskly-this is the direct response to light. Simultaneously, the
other pupil constricts in the same way. This is called the
consensual response to light.
 Move the torch in an arc from pupil to pupil. If an eye has optic
atrophy or severely reduced visual acuity from another cause,
the affected pupil will dilate paradoxically after a short time
when the torch is moved from the normal eye to the abnormal
eye. This is called an afferent pupillary defect (or the Marcus
Gunn pupillary signs). It occurs because an eye with severely
reduced acuity has reduced afferent impulses so that the light
reflex is markedly decreased. When the light is shone from the
normal eye to the abnormal one the pupil dilates, as reflex
pupillary constriction in the abnormal eye is so reduced that
relaxation after the consensual response dominates.

Cranial Nerves III (oculomotor), IV (trochlear) & VI (abducens): The ocular nerves
• Anatomy
o III: Motor function. Nuclei located in periaqueductal gray matter of
midbrain & dorsal to somatic motor nucleus. Emerges from the
midbrain, pierces dura & runs in lateral wall of the cavernous sinus.
Leaves through superior orbital fissure & divides into superior division
& inferior division.
o IV: Somatic motor & proprioreceptor function. Trochlear nucleus
located in periaqueductal grey matter. Emerges from dorsal surface of
midbrain, winds around brainstem, pierces dura & runs along
cavernous sinus, passing through the superior orbital fissure
o VI: Somatic & proprioceptive. Nucleus in pons, emerges from the
brainstem between the pons & medulla & enters pontine cistern,
running alongside basilar artery. Pierces dura & enters orbit through
superior orbital fissure.
• Examination
o Pupils: Examines for size, shape, equality & regularity. Look for ptosis
o Accommodation: Ask patient to look into distance & then focus on an
object 30cm in front of their nose. Normally constriction of both pupils.
Abnormalities with a midbrain lesion, ciliary ganglion lesion,
Parinaud’s syndrome
o Eye Movements: Ask patient to look laterally right and left, then up
and down
o Diplopia: early sign of ocular muscle weakness. If 2 images are side
by side, lateral or medial recti responsible. If one above the other,
obliques or superior or inferior recti responsible
o III nerve lesion: complete ptosis, divergent strabismus, dilated pupil,
unreactive to direct light & accommodation. Commonly related to
trauma, or idiopathic, vascular lesions, compressive lesions,
ischaemia or infarction
o IV nerve lesion: paralysis of superior oblique with weakness of
downward & outward movement. Patient may tilt head to opposite
shoulder. Usually idiopathic or related to trauma
o VI nerve lesion: failure of lateral movement, convergent strabismus &
diplopia. Images horizontal & parallel to each other. Caused by traum,
Wernicke’s encephalopathy, idiopathic or related to trauma
o Nystagmus: disturbance of tone between opposing ocular muscles,
causing sudden quick movement back to original position.
 Jerky horizontal: vestibular lesion, cerebellar lesion, toxins,
internuclear opthalmoplegia
 Jerky vertical: brainstem lesion. Upbeat = midbrain or floor of
4th ventricle. Downbeat = foramen magnum lesion
 Pendular nystagmus: retinal or congenital

Cranial Nerve V: Trigeminal Nerve

• Anatomy
o Sensory & motor fibres
o Its motor nucleus and its sensory nucleus for touch lie in the pons, its
proprioceptive nucleus lies in the midbrain, while its nucleus serving
pain and temperature sensation descends through the medulla to
reach the upper cervical cord. It is the largest of the cranial nerves.
o leaves the pons from the cerebellopontine angle and runs over the
temporal lobe in the middle cranial fossa. At the petrous temporal
bone the nerve forms the trigeminal (Gasserianw) ganglion and from
here the three sensory divisions arise. The first (ophthalmic) division
runs in the cavernous sinus with the third nerve and emerges from the
superior orbital fissure to supply the skin of the forehead, the cornea
and conjunctiva. The second (maxillary) division emerges from the
infraorbital foramen and supplies skin in the middle of the face and the
mucous membranes of the upper part of the mouth, palate and
nasopharynx. The third and largest (mandibular) division runs with the
motor part of the nerve, leaving the skull through the foramen ovale to
supply the skin of the lower jaw and mucous membranes of the lower
part of the mouth
o Pain and temperature fibres from the face run from the pons through
the medulla as low as the upper cervical cord, terminating in the spinal
tract nucleus as they descend. The second order neurones arise in
this nucleus and ascend again as the ventral trigeminothalamic tract.
Touch and proprioceptive fibres terminate in the pontine or main
sensory and mesencephalic nuclei, respectively, to form the dorsal
and ventral mesencephalic tracts. Because of this segregation in the
brainstem, lesions of the medulla or upper spinal cord can cause a
dissociated sensory loss of the face-loss of pain and temperature
sensation, but retention of touch and proprioception.
o Motor fibres supply muscles of mastication
• History
o Pain in distribution of part of trigeminal nerve (trigeminal neuralgia)
o Pontine lesion, compression of trigeminal nerve
o Muscle weakness
• Examination
o Corneal reflex: Lightly touch cornea with a wisp of cotton brought to
eye from side. Reflex blinking of both eyes is normal. Ask patient if
they feel cottonwool. Sensory component mediated by ophthalmic
division of 5th nerve, reflex blink mediated by facial nerve innervation
of orbicularis oculi muscles. If blinking occurs with contralateral eye,
indicates an ipsilateral 7th nerve palsy
o Facial Sensation: 3 divisions of nerve (forehead, cheek, jaw)
o Motor division: Wasting of temporal & masseter muscles (ask patient
to clench teeth & palpate). Ask patient to open mouth & hold it open
while you try to shut it. Unilateral lesion of motor division causes jaw to
deviate towards affected side
o Jaw jerk: Normally slight closure of mouth or no reaction at all. UMNL
above pons jaw jerk is greatly exaggerated
• Causes
o Central: vascular lesion, tumour, syringobulbia
o Peripheral: aneurysm, tumour, chronic meningitis

Cranial Nerve VII: Facial Nerve

• Anatomy
o Nucleus lies in pons next to VI cranial nerve nucleus. Leaves pons
with VII nerve through cerebellopontine angle. After entering the facial
canal it enlarges to become the geniculate ganglion. The branch that
supplies the stapedius muscle is given off from within the facial canal.
The chorda tympani (containing taste fibres from the anterior two-
thirds of the tongue) joins the nerve in the facial canal. The seventh
nerve leaves the skull via the stylomastoid foramen. It then passes
through the middle of the parotid gland and supplies the muscles of
facial expression
• History
o Difficulty speaking, keeping liquids in mouth, facial asymmetry in
o Dryness of eyes or mouth
• Examination
o Facial asymmetry: unilateral drooping of corner of mouth, smoothing
of wrinkled forehead & nasolabial fold. Symmetry maintained with
bilateral palsy
o Muscle power: Ask patient to look up (wrinkling of forehead. Relatively
preserved in UMNL) Ask patient to puff out cheeks, shut eyes tightly,
grin, show teeth. In a LMNL all muscles of facial expression are
affected on the side of the lesion. In Bell’s phenomenon with LMNL
palsy, upward movement of eyeball & incomplete closure of eyelid
when shutting eyes
• Causes
o UMNL: vascular lesion, tumour
o LMNL: Bell’s palsy (most common) vascular lesion, tumour,
syringobulbia, MS, chronic meningitis, fracture, sarcoidosis
o Bilateral facial weakness: Guillain-Barré syndrome, sarcoid, bilateral
parotid disease, Lyme disease or rarely mononeuritis multiplex
o Unilateral loss of taste: middle ear lesions involving chorda tympani or
lingual nerve (rare)

Cranial Nerve VIII: Acoustic Nerve

• Anatomy
o Two components: Cochlear (with afferent fibres subserving hearing) &
vestibular (afferent fibres subserving balance)
o Fibres for hearing originate in organ of Corti & run to cochlear nuclei in
the pons, then there is bilateral transmission to the medical geniculate
bodies & then to superior gyrus of temporal lobes
o Fibres for balance begin in utricle & semicircular canals & join auditory
fibres in facial canal. Enter brainstem at cerevellopontine angle, enter
pons & runs throughout the brainstem & cerebellar
• History
o Loss of hearing (mostly unilateral)
o Trauma, exposure to loud noise etc…
• Examination
o Look to see if patient is wearing hearing aid, remove it. Examine pinna
(scars), pull on pinna gently (tender = external ear disease of
temporomandibular joint disease). Feel for nodes (pre- & post-
auricular = disease of external auditory meatus)
o Otoscope
o Test Hearing: rub fingers next to ear/whisper numbers (68 tests high
tone. 100 tests low tone)
o Rinne’s Test: 256 Hz vibrating tuning fork placed on mastoid process,
when sound is no longer heard, place in line with external meatus.
Nerve deafness- sound audible at external meatus (air & bone
conduction reduced equally) = Rinne +ve. Conduction deafness- no
note audible at external meatus = Rinne –ve
o Weber’s test: 256 Hz tuning fork positioned on centre of forehead.
Nerve deafness- sound heard better in normal ear. Conduction
deafness- sound louder in abnormal ear
• Causes
o Unilateral nerve deafness: tumours, trauma, vascular disease of
internal auditory artery
o Bilateral nerve deafness: environmental exposure to noise,
degeneration, toxicity, infection, Meniere’s disease, brainstem disease
o Conduction deafness: wax, otitis medica, otosclerosis, Paget’s
disease of bone
• Causes of vestibular abnormalities
o Labyrinthine causes: motion sickness, streptomycin toxicity, acute
o Vestibular causes: vestibular neuronitis
o Brainstem causes: vascular lesions, tumours, demyelination, migraine
o Temporal lobe dysfunction

Cranial Nerves IX (Glossopharyngeal) & X (Vagus)

• Anatomy
o Motor, sensory & autonomic functions
o Nerve fibres from nuclei in medulla form multiple nerve rootlets as
they exit the medulla. Join to form IX & X nerves (also contribute to
XI). Nerves emerge from skull through jugular foramen
o IX nerve receives sensory fibres from nasopharynx, pharynx, middle &
inner ear & posterior third of tongue. Carries secretory fibres to parotid
o X nerve receives sensory fibres from pharynx & larynx. Innervates
muscles of pharynx, larynx & palate
• History
o Glossopharyngeal lesion: no definite symptoms. Difficulty in
swallowing dry foods
o Glossopharyngeal neuralgia: tic douloureux. Sudden shooting pains
radiate from one side of throat to ear.
o Unilateral vagus nerve paralysis: difficulty in initiating swallowing of
solids & liquids, hoarseness
• Examination
o Ask patient to open mouth & inspect palate with torch (note uvula
o Ask patient to say ‘ah’. If uvula drawn to one side, indicates a
unilateral X nerve palsy (drawn to normal side)
o Test gag reflex-pressing a stick into the tonsillar fossa will cause
patient to gag. Ask patient if sensation if comparable on both sides.
(IX sensory component. X motor component)
o Ask patient to speak in order to assess hoarseness (X nerve lesion)
• Causes of nerve palsy
o Central: vascular lesions, tumours, syringobulbia, MND
o Peripheral: aneurysms at base of skull, tumours, chronic meningitis,
Guillain-Barre syndrome

Cranial Nerve XI: Accessory Nerve

• Anatomy
o Central portion of nerve arises in medulla close to nuclei of IX, X & XII
nerves. Spinal portion arises from upper 5 cervical segments. Leaves
skull with IX & X nerves through jugular foramen. Central division
provides motor fibres to the vagus & spinal division innervates the
trapezius & sternomastoid muscles
• Examination
o Stand behind patient
o Ask patient to shrug shoulders (test power of trapezius). Feel bulk &
attempt to push shoulders down
o Place hand on lower jaw, ask patient to rotate head against your
resistance to test power of sternomastoid. Feel bulk of muscle on
opposite side
o Torticollis (overactivity of multiple neck muscles) more common than
• Causes of nerve palsy
o Unilateral: trauma, poliomyelitis, basilar invagination, syringomyelia,
o Bilateral: MND, poliomyelitis, Guillain-Barre syndrome

Cranial Nerve XII: Hypoglossal Nerve

• Anatomy
o Nerve arises from medulla. Leaves skull via the hypoglossal foramen.
Motor nerve for tongue
• History
o Difficulty swallowing, sensation of choking
• Examination
o Inspect tongue at rest on floor of mouth (wasting, fasciculations =LMN
o Ask patient to poke tongue straight out (deviates to weaker side if
there is a unilateral LMN lesion. Unilateral UMN lesion causes no
deviation) Clinically obvious UMN lesion is usually bilateral, results in
small, immobile tongue.
o Pseudobulbar palsy = IX, X & XII nerve palsy
o Assess power by asking patient to push tongue against side of cheek
• Causes
o Bilateral UMNL: vascular lesions, MND, tumours
o Unilateral LMNL: vascular lesions, MND, thrombosis of vertebral
artery, syringobulbia. Meningitis, trauma, tumours, lymphadenopathy,
Arnold-Chiari malformation
o Bilateral LMNL: MND, Guillain-Barre syndrome, poliomyelitis, Arnold-
Chiari malformation
o Movement disorders: Parkinson’s (coarse tremor of tongue), athetoid,
choreiform, tardive dyskinesia

Clinical features of pseudobulbar and bulbar palsies

Feature Pseudobulbar (bilateral UMN Bulbar (bilateral LMN lesions
lesions of IX, X and XII) of IX, X and XII)
Gag Increased or normal Absent
Tongue Spastic Wasted, fasciculations
Jaw jerk Increased Absent or normal
Speech Spastic dysarthria Nasal
Other Bilateral limb UMN (long tract) Signs of the underlying cause-
signs e.g. limb fasciculations
Labile emotions Normal emotions
Causes Bilateral cerebrovascular disease Motor neurone disease
(e.g. both internal capsules) Guillain-Barré syndrome
Multiple sclerosis Poliomyelitis
Motor neurone disease Brainstem infarction

Elicit and explain abnormalities of upper and lower limbs

Examination of Upper Limbs

• Observation
o Posture, muscle bulk, abnormal movements, fasciculations

• Tone
o Rotate elbow + wrists with supination and pronation of the elbow joints
at different rates
o The cogwheel rigidity of Parkinson's disease is an important
abnormality of tone in the upper limbs and should be recognised. It is
best assessed by having the patient move the other arm up and down
as the examiner moves the hand and forearm, testing tone at the wrist
and elbow

• Power


• 0 Complete paralysis (no movement).

• 1 Flicker of contraction possible.
• 2 Movement is possible when gravity is excluded.
• 3 Movement is possible against gravity but not if any further resistance is
• 4- Slight movement against resistance.
• 4 Moderate movement against resistance.
• 4+ Submaximal movement against resistance.
• 5 Normal Power

o Shoulder Abduction-mostly deltoid and supraspinatus-(C5, C6): the

patient should abduct the arms with the elbows flexed and resist the
examiner's attempt to push them down.
o Shoulder Adduction-mostly pectoralis major and latissimus dorsi-(C6,
C7, C8): the patient should adduct the arms with the elbows flexed
and not allow the examiner to separate them.
o Elbow Flexion-biceps and brachialis-(C5, C6): the patient should bend
the elbow and pull so as not to let the examiner straighten it out.
o Elbow Extension-triceps brachii-(C7, C8): the patient should bend the
elbow and push so as not to let the examiner bend it
o Wrist Flexion-flexor carpi ulnaris and radialis-(C6, C7): the patient
should bend the wrist and not allow the examiner to straighten it.
o Wrist Extension-extensor carpi group-(C7, C8): the patient should
extend the wrist and not allow the examiner to bend it
o Finger Extension-extensor digitorum communis, extensor indicis and
extensor digiti minimi-(C7, C8): the patient should straighten the
fingers and not allow the examiner to push them down (push with the
side of your hand across the patient's metacarpophalangeal joints).
o Finger Flexion-flexor digitorum profundus and sublimis-(C7, C8): the
patient squeezes two of the examiner's fingers.
o Finger Abduction-dorsal interossei-(C8, T1): the patient should spread
out the fingers and not allow the examiner to push them together.
o Finger Adduction-volar interossei-(C8, T1): the patient holds the
fingers together and tries to prevent the examiner from separating
them further.

• Reflexes

• O absent
• + present but reduced
• ++ normal
• +++ increased, possibly normal
• ++++ greatly increased, often associated with clonus

o Biceps Jerk (C5, C6): place one forefinger on the biceps tendon and
tap with tendon hammer
o triceps jerk (C7, C8), support the elbow with one hand and tap over
the triceps tendon
o Brachioradialis jerk (C5, C6): strike the lower end of the radius above
the wrist

• Coordination
o Finger-nose test: ask patient to touch their own nose, then the
examiner’s forefinger, both briskly and slowly. Look for intention
tremor & past-pointing, which occur with cerebellar disease.
o Rapidly alternating movements: ask patient to pronate & supinate their
hand on the dorsum of the other hand rapidly. Slow & clumsy in
cerebellar disease (called dysdiadochokinesis). Also altered in
extrapyramidal & pyramidal disorders
o Rebound: Ask the patient to lift the arms rapidly from the sides and
then stop. Hypotonia due to cerebellar disease causes delay in
stopping the arms.

• Sensation
o Pain: Test normal area (such as chest). Begin proximally, then test in
each dermatome. Compare right and left sides
o Temperature: Cold sensation can be tested using a metal object
o Vibration: 128 Hz tuning fork. Ask patient to close eyes then place fork
on one of the distal interphalangeal joints. Deaden fork, patient should
be able to say when vibration stops. Compare one side with other.
Move up to ulnar head, elbows, shoulders if abnormalities
o Proprioception: use distal interphalangeal joint of patient’s little finger.
Move it up and down to demonstrate positions, then ask patient to
close their eyes. If abnormality proceed to wrist & elbows
o Light touch: Touch skin with a wisp of cotton wool. Ask patient to close
eyes & say yes when sensation is felt
o C5 supplies the shoulder tip and outer part of the upper arm; C6
supplies the lateral aspect of the forearm and thumb; C7 supplies the
middle finger; C8 supplies the little finger; T1 supplies the medial
aspect of the upper arm and elbow.

Examination of Lower Limbs

• Observation
o Posture, muscle bulk, abnormal movements, fasciculations

• Tone
o Test and knees and ankles
o Clonus: sustained rhythmical contraction of the muscles when put
under sudden stretch. Hypertonia from UMNL. Sharply dorsiflex foot
with knee bent & thigh externally rotated. Test for patellar clonus by
resting hand on lower part of quadriceps with knee extended & move
patella down sharply

• Power
o Hip Flexion-psoas and iliacus muscles-(L2, L3): ask the patient to lift
up the straight leg and not let you push it down (having placed your
hand above the knee).
o Hip Extension-gluteus maximus-(L5, S1, S2): ask the patient to keep
the leg down and not let you pull it up from underneath the calf or
o Hip Abduction-gluteus medius and minimus, sartorius and tensor
fasciae latae-(L4, L5, S1): ask the patient to abduct the leg and not let
you push it in.
o Hip Adduction-adductors longus, brevis and magnus-(L2, L3, L4): ask
the patient to keep the leg adducted and not let you push it out
o Knee Flexion-hamstrings (biceps femoris, semimembranosus,
semitendinosus)-(L5, S1): ask the patient to bend the knee and not let
you straighten it. If there is doubt about the real strength of knee
flexion, it should be tested with the patient in the prone position. Here
possible help from hip flexion is prevented and the muscles can be
palpated during contraction.
o Knee Extension-quadriceps femoris (this muscle is three times as
strong as its antagonists, the hamstrings)-(L3, L4): with the knee
slightly bent, ask the patient to straighten the knee and not let you
bend it.
o Plantar flexion-gastrocnemius, plantaris, soleus-(S1, S2): ask the
patient to push the foot down and not let you push it up.
o Dorsiflexion-tibialis anterior, extensor digitorum longus and extensor
hallucis longus-(L4, L5): ask the patient to bring the foot up and not let
you push it down. The power of the ankle joint can also be tested by
having the patient stand up on the toes (plantar flexion) or on the
heels (dorsiflexion); these movements may also be limited if
coordination is impaired.
o Eversion-peroneus longus and brevis, and extensor digitorum longus-
(L5, S1): ask the patient to evert the foot against resistance.
o Inversion-tibialis posterior, gastrocnemius and hallucis longus-(L5,
S1): with the foot in complete plantar flexion, ask the patient to invert
the foot against resistance

• Reflexes
o Knee jerk (L3, L4). Slide one arm under the knees so that they are
slightly bent and supported. The tendon hammer is allowed to fall onto
the infrapatellar tendon. Normally, contraction of the quadriceps
causes extension of the knee.
o Ankle jerk (S1, S2). Have the foot in the mid-position at the ankle with
the knee bent, the thigh externally rotated on the bed, and the foot
held in dorsiflexion by the examiner. The hammer is allowed to fall on
the Achilles tendon. The normal response is plantar flexion of the foot
with contraction of the gastrocnemius muscle.
o Plantar reflex (L5, S1, S2). After telling the patient what is going to
happen, use a blunt object (such as the key to an expensive motor
car) to stroke up the lateral aspect of the sole, and curve inwards
before it reaches the toes, moving towards the middle
metatarsophalangeal (MTP) joint. The patient's foot should be in the
same position as for testing the ankle jerk. The normal response is
flexion of the big toe at the MTP joint in patients over one year of age

• Coordination
o Heel-shin test. Ask the patient to run the heel of one foot up and
down the opposite shin at a moderate pace and as accurately as
possible. In cerebellar disease the heel wobbles all over the place,
with oscillations from side to side and overshooting.
o Toe-finger test. Unfortunately, a toe-nose test is not a practical way
of assessing the lower limbs, so a toe-finger test is used. Ask the
patient to lift the foot (with the knee bent) and touch the examiner's
finger with the big toe. Look for intention tremor.
o Foot-tapping test. Rapidly alternating movements are tested by
getting the patient to tap the sole of the foot quickly on the examiner's
hand or tap the heel on the opposite shin. Look for loss of rhythmicity.

• Sensation (as for upper limb)

o Pain sensation
o Vibration
o Proprioception (using big toe)
o Light touch
o L2 supplies the upper anterior thigh; L3 supplies the area around the
front of the knee; L4 supplies the medial aspect of the leg; L5 supplies
the lateral aspect of the leg and the medial side of the dorsum of the
foot; S1 supplies the heel and most of the sole; S2 supplies the
posterior aspect of the thigh; S3, S4 and S5 supply concentric rings
around the anus.

(1) Make sure patient’s legs are clearly visible
(2) Ask patient to walk normally for a few metres, then turn and walk towards you
o Assess how quickly the patient is able to start, and how fast they can
turn around (looking for Parkinsonism)
(3) Ask patient to walk heel to toe
o This will aim to exclude a midline cerebellar lesion
(4) Ask patient to walk on toes
o Excludes an S1 lesion
(5) Ask patient to walk on heels
o Exclude L4 and L5 lesion, and this will cause foot drop
(6) Ask the patient to squat and stand
o This will test for proximal myopathy
(7) Romberg test: ask patient to stand erect with feet together. Ask patient to
stand with eyes open and closed for periods of time. Compare steadiness
o Eyes Closed with increased unsteadiness  Proprioceptive
o Eyes Open with increased unsteadiness Cerebellar or vestibular
dysfunction (i.e. balance)

Upper motor neuron lesion

• Lesion has interrupted a neural pathway at a level above the anterior horn
cell: for example, motor pathways in the cerebral cortex, internal capsule,
cerebral peduncles, brainstem or spinal cord.
• Weakness in all muscles. Great weakness of abductors and extensors in the
upper limb & flexors & abductors in the lower limb
• Muscle wasting slight or absent
• Increased tone
• Reflex hyperactivity
• Affected areas
o Monoplegia: motor cortex or partial internal capsule lesion
o Hemiplegia: lesion affecting projection of pathways from contralateral
motor cortex
o Paraplegia: spinal cord trauma
o Quadriplegia: Spinal cord trauma or brainstem lesion
• Causes
o Vascular disease: Lesions in internal carotid artery result in
hemiplegia on opposite side of body. Homonymous hemianopia,
hemianaesthesia & dysphasia may occur. Lesions in vertebrobasilar
artery produce cranial nerve palsies, cerebellar signs, Horner’s
syndrome & sensory loss
o Compressive & infiltrative lesions: Occur in lobes of brain. Focal signs
depend on tumour site
o Demyelinating disease: MS
o Infection: HIV

Lower motor neuron lesion

• Lesions interrupt the spinal reflex arc (occur in spinal motor neurons, motor
root or peripheral nerve)
• Loss of strength
• Muscle wasting
• Reduced tone
• Reduced or absent reflexes
• Fasciculations

Cerebellar disorders
• History
o Clumsiness, problems with coordination (signs occur on same side as
lesion in brain because fibres cross twice in brainstem)
• Examination
o Nystagmus
o Jerky, explosive & loud speech, with irregular separation of syllables
o Arm drift due to hypotonia of agonist muscles
o Hypotonia
o Abnormal finger-nose, rapidly alternating movements & rebound tests
o Abnormal gait
• Types
o Midline lesion: truncal ataxia, abnormal hell-toe walk, abnormal
o Bilaternal disease: Hypotonia, abnormal gait, nystagmus

Mini-Mental State Examination


1. Ask the date. Then ask specifically for parts omitted, for example, 'Can you also
tell me what season it is?' Score 1 point for each correct. 2. Ask in turn, 'Can you tell
me the name of this place?' (town, country, etc). Score 1 point for each correct.

Ask the patient if you may test his or her memory. Then say the names of three
unrelated objects, clearly and slowly, about one second for each. After you have said
all three, ask him or her to repeat them. This first repetition determines the score (0-
3) but keep saying them until he or she can repeat all three, up to six trials. If he or
she does not eventually learn all three, recall cannot be meaningfully tested.

Attention and calculation

Ask the patient to begin with 100 and count backwards by 7. Stop after five
subtractions (93, 86, 79, 72, 65). Score the total number of correct answers. If the
patient cannot or will not perform this task, ask him or her to spell the word 'world'
backwards. The score is the number of letters in correct order, eg dlrow 5, dlowr 3.

Ask the patient if he or she can recall the three words you previously asked him or
her to remember. Score 0-3.

Naming: Show the patient a wrist-watch and ask him or her what it is. Repeat for
pencil. Score 0-2.

Repetition: Ask the patient to repeat the sentence after you. Allow only one trial.
Score 0 or 1.

Three-stage command: Give the patient a piece of plain blank paper and repeat the
command. Score 1 point for each part correctly executed.
Reading: On a blank piece of paper, print the sentence 'Close your eyes' in letters
large enough for the patient to see clearly. Ask him or her to read it and do what it
says. Score 1 point only if he or she actually closes his eyes.

Writing: Give the patient a blank piece of paper and ask him or her to write a
sentence for you. Do not dictate a sentence, it is to be written spontaneously. It must
contain a subject and verb and be sensible. Correct grammar and punctuation are
not necessary.
Copying: On a clean piece of paper, draw intersecting pentagons (as below), each
side about one inch and ask him or her to copy it exactly as it is. All ten angles must
be present and two must intersect to score 1 point. Tremor and rotation are ignored.

A score of 20 or less generally suggests dementia but may also be found in acute
confusion, schizophrenia or severe depression. A score of less than 24 may indicate
dementia in some patients who are well educated and who do not have any of the
above conditions. Serial testing may be of value to demonstrate a decline in cognitive
function in borderline cases.

Cerebrovascular Accident


• Stroke. To the public, stroke means weakness, either permanent or transient

on one side, often with loss of speech. Stroke is defined as the clinical
syndrome of rapid onset of cerebral deficit (usually focal) lasting more than 24
hours or leading to death, with no apparent cause other than a vascular one.
Hemiplegia following middle cerebral arterial thromboembolism is the typical
• Completed stroke means the deficit has become maximal, usually within 6
• Stroke-in-evolution describes progression during the first 24 hours.
• Minor stroke. Patients recover without significant deficit, usually within a
• Transient ischaemic attack (TIA). This means a focal deficit, such as a
weak limb, aphasia or loss of vision lasting from a few seconds to 24 hours.
There is complete recovery. The attack is usually sudden. TIAs have a
tendency to recur, and may herald thromboembolic stroke.
• CVA is defined as:
- The sudden onset of a focal neurological deficit resulting from either infarction
or hemorrhage within the brain
- Adults 45 years old most likely to have a cardiac source of embolism
- System(s) Affected: Cardiovascular; Nervous
- Synonym(s): Cerebrovascular accident; Reversible ischemic neurological

Geriatric Considerations
Amyloid (congophilic) angiopathy is most prevalent in the elderly, especially if the patient also
has dementia.

Pediatric Considerations
Cardiac (especially developmental abnormalities)
Metabolic: Homocystinuria, Fabry disease

Pregnancy Considerations
Parturition may increase the risk of rupture for aneurysm; amniotic fluid embolism may cause
stroke at the time of delivery.
Postpartum period is associated with an increased risk for cerebral venous thrombosis.

General prevention
Stop smoking.
Control blood pressure, diabetes, hyperlipidemia
Use alcohol in moderation, if at all.
Regular exercise
Maintain positive psychological outlook.
Maintain weight control.
Antiplatelet drugs
Angiotensin-converting enzyme inhibitors
Treat homocystinemia with vitamin B6, vitamin B12, and folic acid.
Anticoagulation when cardioembolism is the suspected cause


Predominant age: Risk increases over age 45 and is highest in the seventh and
eighth decades
Predominant sex: Male > Female (3:1), but equalises after menopause.

Risk factors
- Age
- Hypertension
- Cardiac disease
- Smoking
- Diabetes
- Antiphospholipid antibodies
- Family history
- Atrial fibrillation
- Hyperlipidemia
- Homocystinemia

Inheritance is polygenic with a tendency to clustering of risk factors within families.

Ischemic: Carotid atherosclerotic disease with artery-to-artery thromboembolism
-Cardioembolism secondary to valvular (mitral valve) pathology
-Mural hypokinesias or akinesias with thrombosis (acute anterior myocardial
infarctions or congestive cardiomyopathies)
-Cardiac arrhythmia (atrial fibrillation)
Hypercoagulable states:
-Antiphospholipid antibodies, factor V Leiden deficiency, deficiency of protein S,
-Presence of antithrombin 3, oral contraceptives
Other causes:
-Spontaneous and post-traumatic (i.e., chiropractic manipulation) artery dissection
-Fibromuscular dysplasia
-Drugs (cocaine, amphetamines)
Hypertension: May cause damage to putamen, internal capsule, cerebellum,
brainstem, corona radiata
Amyloid (congophilic) angiopathy: Lobar (cortical) hemorrhages in the elderly
Vascular malformations: Arteriovenous malformation, cavernous angioma, venous
angioma, and capillary angioma

Associated Conditions
The major cause of death in the first 5 years after a stroke is cardiac disease.

Signs and Symptoms
 Carotid circulation (hemispheric): Hemiplegia, hemianesthesia, neglect, aphasia,
visual field defects; less often headaches, seizures, amnesia, confusion
 Vertebrobasilar (brainstem or cerebellar): Diplopia, vertigo, ataxia, facial paresis,
Horner syndrome, dysphagia, dysarthria
 Impaired level of consciousness
 Cerebellar lesion in patients with headache, nausea, vomiting, and ataxia

Special tests:
 Duplex carotid ultrasonography
 Cerebral angiography
 Transthoracic echocardiogram; if normal and a cardiac source is suspected, follow
up with transesophageal echocardiogram
 Holter monitoring
 EEG for suspected seizure
 Prothrombin time (PT) and partial thromboplastin time (PTT); Coumadin prolongs
 Antiphospholipid antibodies
 Cardiac enzymes

Acute phase:
 CT of head
 MRI scan of brain with diffusion-weighted imaging, magnetic resonance
angiography of brain and neck vessels

 Migraine
 Focal seizure
 Tumor
 Subdural hematoma
 Hypoglycemia, hyperglycemia, hypercalcemia


 Acute phase: Inpatient care, preferably in a stroke unit

 Surgical therapy:
-In medically fit patients with nondisabling stroke, carotid endarterectomy is
indicated for stenosis of >70% on side ipsilateral to stroke.
-Medical therapy for 50% stenosis, 50-69% depends on risk factors

General Measures
 Maintain oxygenation.
 Monitor cardiac rhythm for 48 hours.
 Control hyperglycemia (keep glucose 220 mg/dL [12.1 mmol/L]).
 Treat blood pressure >185/110 if patient will be or has been treated with IV tissue
plasminogen activator.
 Do not treat elevated blood pressure unless acute end-organ dysfunction
(encephalopathy, myocardial ischemia, aortic dissection, acute renal failure).
 Prevent hyperthermia
 Early introduction of physiotherapy and ambulation
 Heparin 5,000 units SC q12h
 Alert with no dysphagia: Diet as tolerated (no added salt if hypertensive)
 Alert with dysphagia: Pureed dysphagia diet or nasogastric feeding tube if

Ambulate as soon as possible.


First Line
 IV tissue plasminogen activator 0.9 mg/kg in highly selected cases within 3 hours
of ischemic stroke
 Enteric-coated aspirin 50-325 mg per day or Dipyridamole-aspirin (Aggrenox):
extended release
 Clopidogrel (Plavix):
 Warfarin

Follow Up

 Variable depending on severity of stroke
 Posterior circulation strokes have a higher acute mortality rate, but generally make
a better functional recovery than hemispheric strokes.

 Shoulder subluxation
 Hyperextension knee injury
 Depression
 Sympathetic dystrophy

Patient Monitoring
Follow the patient every 3 months for the first year, then yearly.
Parkinson Disease

An adult-onset neurodegenerative disorder of the extrapyramidal system
characterized by a combination of tremor at rest, rigidity, and bradykinesia
- Diagnosis requires therapeutic response to levodopa, which implies normal striatal
- Only neurodegenerative disease treatable long term
- System(s) Affected: Musculoskeletal; Nervous
- Synonym(s): Paralysis agitans; Shaking palsy

Predominant age: 60 years, with 5% between the ages of 21-39
Predominant sex: Male > Female (1.4:1)

In ages 55-64, 0.3%
In ages 65-74, 1%
In ages 75-84, 3.1%
In ages 85-94, 4.3%

Geriatric Considerations
Common among elderly

Paediatric Considerations
May occur as secondary parkinsonism in this age group
Risk Factors
Unknown in the idiopathic disease
Association between smoking and increased caffeine intake and reduced risk for
Parkinson disease has been reported.

May be a genetic role, with risk 2.95-fold in patients with positive family history in
late-onset disease, 7.76-fold increase in early-onset disease (age 50 years)

 Unknown
 Loss of dopaminergic neurons in the substantia nigra, with rate of loss 1% per
year in patients with Parkinson vs. 0.5% in normal aging
 No clear environmental causes identified
 Known toxins: MPTP, pesticides. Other nondopaminergic neurons may be

Associated Conditions
 Psychosis
 Depression


Signs and Symptoms

 Cardinal signs:
-Tremor (4-8 Hz) in repose: Diagnostic, but not required; relieved with activity,
concentration, and sleep; increases with stress; 10% of patients present with only
tremor, 30% present without; most begin with unilateral tremor
-Bradykinesia: Required for diagnosis; most disabling symptom; movement initiation
difficult, causes the gait and postural abnormalities; fine, repetitive movements
affected more than large
-Rigidity: Lead-pipe type; cogwheel with tremor
 Common presentation:
-Asymmetric tremor
-Clumsy or weak limb: Early sign of bradykinesia
-Stiff or uncomfortable limb: Early rigidity
-Gait disorder: Asymmetric slowness, shuffling, reduced arm movement or
 Other associated signs and symptoms:
-Speech is poorly enunciated, low volume, clipped
-Ocular abnormalities: Decreased blinking, blepharospasm, impaired upward gaze
-Dysautonomia with constipation, incontinence, sexual dysfunction
-Depression in 2/3 of patients
-Dementia in 20% of patients mild to moderate
-Gait disturbances including no arm swing, en mass turning, problems getting up
from chair, festination, freezing
-Leaning posture
-Propulsion or retropulsion
-Mask faces
-Neglect of swallowing with drooling
 Hoehn and Yahr scale of disability:
-Stage 1: Unilateral, minimal functional impairment
-Stage 2: Bilateral, without impairment of balance
-Stage 3: Bilateral, positive instability; patient is physically independent
-Stage 4: Severe disability; patient can walk or stand without assistance, but is
markedly incapacitated
-Stage 5: Patient is wheelchair bound or bedridden unless aided

Physical Exam
Diagnostic criteria:
 Clinically definite if any 3 of the following are present or any 2 of the 1st 3 display
-Rest tremor
-Impaired postural reflexes
 CT or MRI to help rule out other disorders
 Positron emission tomography scanning

Pathological Findings
Lewy bodies

 Parkinsonism: Bradykinesia with little or no response to levodopa, indicating that
the striatal neurons are also degenerated:
-Progressive supranuclear palsy
-Multisystem atrophy
-Alzheimer with extrapyramidal features
-Side effects of neuroleptic medications
-Infectious postencephalitic
-Vascularlacunar state
-Metabolic Wilson disease: Onset at age 40
 Benign essential tremor: Positive family history and relief with alcohol
 Consider other conditions if:
-Falls or early dementia
-Symmetric Parkinsonism
-Wide-based gait
-Abnormal eye movements
-Orthostatic hypotension
-Babinski sign
-Urinary retention
-Rapid progression


General Measures
 Drugs have therapeutic and toxic effects.
 Acute worsening may indicate depression, noncompliance, or supervening illness.
 Course is progressive with or without drugs. Lifelong therapy directed toward
symptom control treat disability
 Investigate for drug-induced cause; if found, discontinue drug. Symptom
resolution may take weeks to months.

 Small, frequent meals if difficulty in eating
 High liquid intake important; high-bulk foods
 Reduced-protein diet is unnecessary

Maintain activity at whatever level possible; use cane for walking


First Line
 Levodopa/carbidopa (Sinemet): Most effective and the initial drug of choice in
older patients with more severe symptoms, speech disorders and falls are resistant
to levodopa:
 Dopamine agonists slightly less effective; long half-life; reduces wearing-off
effects of levodopa. Add when levodopa >500 mg per day. Early monotherapy may
reduce levodopa use and long-term side effects. May be initial drug of choice in
younger patients with milder symptoms. Usually need addition of levodopa in 1st 5
years of monotherapy. Avoid with dementia

Adjuvant Drugs
 Tricyclic antidepressants for nighttime sedation and associated depression (50%
of patients with Parkinson)
 Apomorphine as agonist or for freezing (use limited by adverse effects [vomiting]
and need for parenteral administration)
 Clozapine: 70-200 mg suppress frequency of dyskinesia and increase "on" time;
also useful for hallucinations (50 mg/day). Side effects include sedation, sialorrhea,
and agranulocytosis.
 Donepezil: 5 mg; cognitive impairment
 Modafinil: 100-200 mg excessive daytime sleepiness

 Adrenal medullary transplants unproven
 Thalamotomy akinesia
 Stereotactic pallidotomy akinesia
 Deep brain stimulation of subthalamic nucleus dyskinesia, tremor response 88%;
may worsen pre-existing psychiatric disorders; fewer "off" problems, fewer "on"
dyskinesias, and 50% reduction of medications

Follow up

 More rapid progression: Older at disease onset; dementia
 Milder disease: Predominant feature is tremor

 Aspiration pneumonia
 Falls
 Associated with a 2-fold increase in risk of death

Patient Monitoring


A pathologic process defined as a persistent impairment of a prior level of intellectual
 Alzheimer dementia (AD):
-Characterized by relentless deterioration of higher cortical functioning
-Variable rate of deterioration
 Vascular dementia (VaD):
-Formerly multi-infarct dementia
-Caused by clinical or subclinical cerebral infarcts secondary to atherosclerosis
-Stepwise deterioration with periods of clinical plateaus
 Dementia with Lewy bodies (DLB):
-Early-onset dementia with associated psychosis, depression
 Frontotemporal dementia (FTD):
-Insidious change in personality with cognitive dysfunction
-Onset usually prior to age 65

General prevention
Ischemic-vascular dementia: General stroke prevention (lipid, diabetes, blood
pressure control)

Predominant age: Increasing incidence with increasing age
Predominant sex: Male = Female

Between ages 60-64 years: 0.5%
Between ages 80-90 years: 3.2%

Risk factors
Increasing age
Prevalence of atherosclerotic disease (VaD)
History of head trauma
History of CNS infection
Midlife depression (VaD)

At least 15% of patients with AD will report a positive family history
Persons with Trisomy 21 (Down syndrome) who survive into their 20s and 30s will
inevitably develop a progressive dementia

 AD:
-Genetic predisposition in more than 15%
 VaD
-Cerebral atherosclerosis or emboli with clinical or subclinical infarcts
 Secondary dementias: Causes include hypothyroidism, vitamin B deficiency,
normal pressure hydrocephalus, AIDS, syphilis, and various medications.


Signs and Syptoms

 Impaired short-term and long-term memory
 Impaired abstract thinking
 Impaired judgment
 Aphasia
 Apraxia
 Agnosia
 Anomia
 Personality change, emotional outbursts, wandering, restlessness, hyperactivity,
especially with FTD
 Sleep disturbances
 Mood disturbances
 Urinary incontinence (usually late in AD or normal pressure hydrocephalus)
 Fecal incontinence (late)
 Rigidity
 Tremor (especially with DLB)
 Hallucinations (especially with DLB)
 Delusions
 Overt paranoid behavior
 Weight loss
 Seizures

 Mental status testing
 Neuropsychologic testing
 Electroencephalogram for patients with altered consciousness or associated

Done primarily to rule out potentially reversible causes:
 Thyroid function tests
 Syphilis serology
 Serum B12 and folate levels
 CBC and screening metabolic profile
 Drugs that may alter lab results: Thyroid hormone replacement and iodine
preparations may affect thyroid function tests.
 Disorders that may alter lab results: False positive syphilis serology with acute
infections, leprosy, subacute bacterial endocarditis, and autoimmune disorders

 Head CT if history suggestive of a mass, or focal neurologic signs or in patient
with dementia of brief duration
-More sensitive than CT for detection of soft-tissue lesions (small infarcts, mass
lesions, atrophy of the brainstem, and other subcortical structures).
-May also clarify ambiguous CT findings.
 Isotope cisternography if suspicious of normal pressure hydrocephalus
 Positive emission tomography shows cortical hypometabolism

Pathological Findings
 AD:
-Diffuse cerebral atrophy in association areas, hippocampus, amygdala
-Granulovesicular degeneration
-Neurofibrillary tangles
-Senile neuritic plaques
-Microvascular amyloid
 VaD:
-Old infarcts, lacunes
-Manifestations of atherosclerotic disease

 Delirium
 Normal aging
 Mild cognitive impairment
 Depression
 Schizophrenia
 Chronic alcoholism
 Postsurgical and/or postanesthesia state
 Normal Pressure Hydrocepahalus


General Measures
 Daily schedules and written directions
 Support and education of caregivers
 Emphasis on nutrition, personal hygiene, personal safety (accident-proofing the
home), and supervision
 Discussions with the family concerning advance directives
 Socialization (adult day care)
 Sensory stimulation (prominent displays of clocks and calendars)
 Improvement in sleep hygiene
 Pharmacotherapy should be reserved for specific behavioral symptoms after non-
pharmacologic therapy has failed

No special diet

Fully active with direction and supervision


 Aggressive behaviors: Antipsychotics such as risperidone (Risperdal) 0.5-1.0 mg,

olanzapine (Zyprexa) 2.5 mg, or quetiapine (Seroquel) 25 mg PO at bedtime are
reasonable choices in a non-emergency situation (3)[B]. Other options include
carbamazepine (Tegretol) 100 mg b.i.d.-t.i.d. or Valprioc acid 250-1,500 mg daily in
divided dose
 Depression: Use serotonin reuptake inhibitors: Sertraline (Zoloft), fluoxetine
(Prozac), paroxetine (Paxil), citalopram (Celexa), or escitalopram (Lexapro) all orally.
Start with half the usual starting dose.
 Sleep disturbance: Intermittent use of temazepam (Restoril) 7.5-15 mg, zolpidem
(Ambien) 5 mg, trazodone (Desyrel) 25-50 mg, or mirtazapine (Remeron) 7.5 mg at
bedtime is occasionally warranted
 Cognitive dysfunction: Donepezil (Aricept) 5-10 mg daily, rivastigmine (Exelon)
1.5-6 mg b.i.d., galantamine (Reminyl) 4-12 mg (4)[B], memantine (Namenda) 5-20
mg daily PO

 AD: A progressive disease with variable rates of progression, but inevitably
leading to profound cognitive impairment
 VaD: Less likely to be progressive, but cognitive improvement is unlikely
 Secondary dementias: Treatment of the underlying condition may lead to

Patient Monitoring
 Periodic mental status testing to assess progression and predict prognosis
 Periodic monitoring of nutritional status
 Periodic monitoring of the caregiver status to assess for caregiver stress
 Periodic assessment of the environment for safety
Cerebella Disorders

The third system of motor control modulates coordination, rather than speed. Ataxia,
i.e. unsteadiness, is characteristic when it malfunctions.
The cerebellum receives afferent fibres from:

• proprioceptive receptors in joints and muscles

• vestibular nuclei
• basal ganglia
• the corticospinal system
• olivary nuclei.

Efferent fibres pass from the cerebellum to:

• each red nucleus

• vestibular nuclei
• basal ganglia
• corticospinal system.

Each lateral cerebellar lobe coordinates movement of the ipsilateral limbs. The
vermis (a midline structure) is concerned with maintenance of axial (midline) posture
and balance.

Cerebellar lesions

Expanding mass lesions within the cerebellum obstruct the aqueduct to cause
hydrocephalus, with severe pressure headaches, vomiting and papilloedema. Coning
of the cerebellar tonsils through the foramen magnum and respiratory arrest occur,
often within hours. Rarely, tonic seizures (sudden attacks of limb stiffness) occur.

Lateral cerebellar lobes

A lesion within one cerebellar lobe (e.g. a tumour or infarction) causes disruption of
the normal sequence of movements (dyssynergia) on the same side. Ataxia and
other signs develop.
A lesion within one cerebellar lobe (e.g. a tumour or infarction) causes disruption of
the normal sequence of movements (dyssynergia) on the same side. Ataxia and
other signs develop. Neurotransmitter changes in cerebellar disease are poorly

Posture and gait

The outstretched arm is held still in the early stages of a cerebellar lesion (cf. the drift
of a pyramidal lesion) but there is rebound upward overshoot when the limb is
pressed downwards and released. Gait becomes broad and ataxic; the patient falters
towards the lesion.

Tremor and ataxia

Movement is imprecise in direction, in force and in distance (dysmetria). Rapid

alternating movements (tapping, clapping or rotary hand movements) are clumsy and
disorganized (dysdiadochokinesis). Intention tremor (action tremor, with past-
pointing) is seen. Speed of movement is preserved, cf. extrapyramidal disease.


Coarse horizontal nystagmus develops with lateral cerebellar lobe lesions - the fast
component towards the lesion.


A halting, jerking dysarthria occurs - the scanning speech of cerebellar lesions

(usually bilateral).
Other signs

Principal causes of cerebellar syndromes

Tumours Haemangioblastoma
Secondary neoplasm
Compression by acoustic neuroma
Vascular lesions Haemorrhage
Arteriovenous malformation
Infection Abscess
Developmental Arnold-Chiari malformation
Basilar invagination
Cerebral palsy
Toxic and metabolic Anticonvulsant drugs
Chronic alcohol abuse
Following carbon monoxide poisoning
Lead poisoning
Solvent abuse
Inherited Friedreich's ataxia
Ataxia telangiectasia
Essential tremor
Miscellaneous Multiple sclerosis
Postinfective cerebellar syndrome of childhood
Non-metastatic manifestation of malignancy
Cerebral oedema of chronic hypoxia

Titubation - rhythmic head tremor in either to and fro ('yes-yes') movements or

rotary ('no-no') movements - also occurs, mainly when cerebellar connections are
involved (e.g. in essential tremor and MS). Hypotonia (floppy limbs) and depression
of reflexes (and slow, pendular reflexes) are also sometimes seen with cerebellar
disease, though of little value as localizing signs.
Midline cerebellar lesions

Midline cerebellar vermis lesions have a dramatic effect on trunk and axial
musculature-difficulty standing and sitting unsupported, with a rolling, broad, ataxic
gait (truncal ataxia). Lesions of the flocculonodular region of the cerebellum cause
vertigo, vomiting and gait ataxia if they extend to the roof of the fourth ventricle.


Tremor means a regular and sinusoidal oscillation. Different varieties are outlined
below. Pathological anatomy and neurotransmitter changes remain largely unknown.

Postural tremor

Everyone has a physiological tremor (often barely perceptible) of the outstretched

hands at 8-12 Hz. This is increased with anxiety, caffeine, hyperthyroidism and
certain drugs (sympathomimetics, sodium valproate, lithium) or in mercury poisoning.
A coarser, postural tremor is seen in benign essential tremor (usually at 5-8 Hz) and
in chronic alcohol abuse. Postural tremor does not worsen on movement, though it
may become more obvious.

Intention tremor

Tremor exacerbated by action, with past-pointing and accompanying incoordination

of rapid alternating movement (dysdiadochokinesis), occurs in cerebellar lobe
disease and with lesions of cerebellar connections. Titubation and nystagmus may
be present.

Rest tremor
This tremor occurs typically in Parkinson's disease, and is noticeably worst at rest,
usually between 4 and 7 Hz - 'pill-rolling' between thumb and index finger.

Other tremors

Coarse tremor is seen following lesions of the red nucleus (e.g. infarction,
demyelination) and rarely with frontal lobe lesions.

Peripheral Nerve Disease

The various nerve fibre types are shown in the table below. All are myelinated except
C fibres that carry impulses from pain receptors.

A, B and C fibres in peripheral nerves

(μ) Conduction velocity m/s Function
Aα(1-20) 70-110 Motor; proprioception
Aβ(5-10) 30-60 Touch
Aγ(3-6) 20-30 Fusimotor, to spindles
Aδ(2-5) 20-30 Sharp pain
B (< 3) 5-15 Autonomic, preganglionic
C (< 1.3) 0.5-2 Slow pain

Mechanisms of damage to peripheral nerves

Peripheral nerves consist of two principal cellular structures - the axon and its
anterior horn cell, and the myelin sheath, produced by Schwann cells between each
node of Ranvier. Blood supply is via vasa nervorum. Six principal mechanisms, some
coexisting, cause nerve malfunction.

1. Demyelination

When the Schwann cell is damaged, the myelin sheath is disrupted. This causes
marked slowing of conduction, seen for example in Guillain-Barré syndrome, post-
diphtheritic neuropathy and many hereditary sensorimotor neuropathies.

2. Axonal degeneration

The primary damage is in the axon, which dies back from the periphery. Conduction
velocity tends to remain normal because axonal continuity is maintained in surviving
fibres. Axonal degeneration occurs typically in toxic neuropathies.

3. Wallerian degeneration

This describes the changes following nerve section. Both axon and distal myelin
sheath degenerate over several weeks.

4. Compression

Focal demyelination at the point of compression. The myelin sheath is disrupted.

This occurs typically in entrapment neuropathies e.g. carpal tunnel syndrome.
5. Infarction

Microinfarction of vasa nervorum occurs in arteritis, e.g. polyarteritis nodosa, Churg-

Strauss syndrome, and in diabetes mellitus. Wallerian degeneration occurs distal to
the ischaemic zone.

Nerve regeneration

Regeneration occurs either by remyelination, when recovering Schwann cells spin

new myelin sheaths around the axon, or by axonal growth down the nerve sheath
and sprouting from the axonal stump. Axonal growth takes place at a rate of up to 1
mm daily.


• Peripheral neuropathies - The type of neuropathy (axonal or demyelinating)

can be assessed by electrical nerve studies. Neuropathy means a
pathological process affecting a peripheral nerve or nerves.
• Mononeuropathy means a process affecting a single nerve.
• Mononeuritis multiplex (multiple mononeuropathy, or multifocal neuropathy)
affects several or multiple nerves.
• Polyneuropathy describes diffuse, symmetrical disease, usually beginning
peripherally. The course is either acute, chronic, static, progressive, relapsing
or towards recovery. Polyneuropathies are motor, sensory, sensorimotor (i.e.
mixed) and autonomic. They are classified broadly into demyelinating and
axonal types, depending upon which principal pathological process
predominates. It is often impossible to separate these clinically. Many
different classifications exist. Many systemic diseases cause neuropathies.
Widespread loss of tendon reflexes is typical.
• Radiculopathy means disease affecting nerve roots.
Diagnosis is made by clinical pattern, electrical tests, nerve biopsy (usually sural or
radial) and identification of systemic or genetic disease.


· A neurologic complication of illness and/or medication(s) especially common in
older patients
· A medical emergency requiring immediate evaluation to decrease morbidity and
· System(s) Affected: Nervous
· Synonym(s): Acute confusional state; Altered mental status; Organic brain
syndrome; Acute mental status change

· Predominant age: Older persons
· Predominant sex: Male = Female

· 25-60%
· >50% in high-risk older patients
10-40% in hospitalised older patients

Risk Factors
Predisposing risk factors:
· Advanced age
· Prior cognitive impairment
· Functional impairment
· High blood urea nitrogen (BUN): Creatinine ratio
· Dehydration
· Malnutrition
· Hearing or vision impairment
· Frailty Precipitating risk factors:
· Severe illness in any organ system(s)
· Need for a urinary catheter
· >3 medications
· Pain
· Any adverse iatrogenic event
· Medications, especially long-acting sedative hypnotics (e.g., diazepam and
flurazepam), narcotics (especially meperidine), and anticholinergics (especially

· Neuropathophysiology is not clearly defined
· Multicomponent approach addressing contributing factors can reduce incidence and

Usually multifactorial:
· Often interaction between predisposing and precipitating risk factors
· With more predisposing factors (i.e., the frailer the patients), fewer precipitating
factors needed to produce delirium
· If few predisposing factors (e.g., very robust patients) more precipitating factors
needed to manifest delirium

Associated Conditions
Multiple, but most common are
· New medicine or medicine changes
· Infections (especially lung and urine, but meningitis needs consideration as welll)
· Toxic-metabolic (Especially low sodium, elevated calcium, renal failure and hepatic
· Heart attack
· Stroke
· Alcohol or drug withdrawal


The Confusion Assessment Method (CAM - Mini Mental) may be applied either pre-
hospital or in hospital, and has been adapted for the ICU setting (CAM-ICU)

· Key diagnostic features comprise the CAM.
-Acute change in mental status that fluctuates
-Abnormal attention
-and either disorganized thinking or altered level of consciousness
· Any of the following non-diagnostic symptoms may be present:
-Short- and long-term memory problems
-Sleep-wake cycle disturbances
-Hallucinations and/or delusions
-Emotional lability
-Tremors and asterixis
· Subtypes based on level of consciousness:
-Hyperactive delirium (15%): Patients are loud, rambunctious, and disruptive.
-Hypoactive delirium (20%): Quietly confused; may sit and not eat, drink, or move
-Mixed delirium (50%): Features of both hyperactive and hypoactive delirium
-Normal consciousness delirium (15%): Still display disorganized thinking, along
with acute onset, inattention, and fluctuation.

· Time course of mental status changes
· Recent medication changes
· Symptoms of infection
· New neurologic signs

Physical Exam
· Good cardiorespiratory exam essential
· Focal neurologic signs usually absent
· Mini-mental state exam helpful as structured interview and to follw course over time

ECG as necessary

· Electrolytes, BUN, and creatinine
· Urinalysis, urine culture
· If needed:
-Arterial blood gases
-Drug screen
-Liver function tests
· Chest radiograph
· Non-contrast-enhanced head (CT) scan if:
-Unclear diagnosis
-Recent fall
-Receiving anticoagulants
-New focal neurologic signs
-To rule out increased intracranial pressure before lumbar puncture

Diagnostic Procedures/Surgery
Lumbar puncture:
· Rarely necessary
· Perform if clinical suspicion of a CNS bleed or infection is high.

· Depression (slow onset, disturbance of mood, normal level of consciousness, and
fluctuates over weeks to months)
· Dementia (insidious onset, memory problems, normal level of consciousness, and
fluctuates over days to weeks)
· Psychosis (rarely sudden onset in older adults)


· Stabilise vitals if needed.
· Ensure immediate evaluation.

General measures
· Postoperative patients should be monitored and treated for the following:
-Myocardial infarction/ischemia
-Pulmonary complications/pneumonia
-Pulmonary embolism
-Urinary or stool retention (attempt catheter removal by postoperative day 2)
· Anesthesia route (general epidural) does not affect the risk of delirium
· Multifactorial treatment: Identify contributing factors and provide pre-emptive care to
avoid iatrogenic problems (2-4)[A] with special attention to:
· Central nervous system oxygen delivery (attempt to attain the following):
-SaO2 >90% with goal of SaO2 >95%
-Systolic blood pressure <2/3 of baseline or >90 mm Hg
-Hematocrit >30%
· Fluid/electrolyte balance:
-Sodium, potassium, and glucose normal (glucose <300 mg/dL in diabetics)
-Treat fluid overload or dehydration
· Treat pain:
-Schedule acetaminophen (1 g q.i.d.) if daily pain
-Morphine or oxycodone for breakthrough pain if acetaminophen ineffective

Avoid meperidine (Demerol)

· Eliminate unnecessary medications:

-Investigate new symptoms as potential medication side effects
· Regulate bowel/bladder function:
-Bowel movement at least every 48 hours
-Screen for urinary retention or incontinence, especially after catheter removal
· Prevent major hospital-acquired problems:
-6-inch-thick foam mattress overlay or a pressure-reducing mattress
-Avoid urinary catheter
-Incentive spirometry, if bed bound
-Subcutaneous heparin 5,000 u b.i.d., if bedfast
· Environmental stimulation:
-Glasses and hearing aids
-Clock and calendar
-Soft lighting
-Radio, tapes, and television, if desired
· Sleep:
-Quiet environment
-Soft music
-Therapeutic massage
· Restraints do not reduce risk of falls/injury:
-Use only in the most difficult-to-manage patients, as briefly as possible
· Dentures used properly
· Proper positioning for meals
· Assistance with meals when necessary
· Nutritional supplements (1-3 cans daily) if intake is poor
· Temporary nasogastric tube if unable to eat and bowels working

· As tolerated
· Early physical therapy consultation to prevent deconditioning

· IInstitute skin care program for patients with established incontinence
· Turning regimen if at risk of pressure ulcers

Special Therapy

Physical Therapy
Early mobilization critical:
· Out of bed on hospital day 2 (or postoperative day 1) if no contraindications
· Out of bed several hours daily if able
· Daily therapy if not ambulating independently
· Daily therapy if not functionally independent

IV Fluids
As needed for dehydration

· Nonpharmacologic approaches are preferred for initial treatment
· Medications often treat only the symptoms and do not address the underlying cause

First Line
· Neuroleptics:
-Haloperidol (Haldol): initially, 0.25-0.5 mg PO/IM/IV unless urgent sedation needed
-Quetiapine (Seroquel): 25 mg daily to b.i.d.
· Short-acting benzodiazepines, if neuroleptics do not work or should be avoided:
-Lorazepam (Ativan): initially, 0.25-0.5 mg PO/IM/IV q6-8h, may need to adjust to
effect (caution in patients with impaired liver function).
· Risperidone (Risperdal): 0.25-0.5 mg PO daily
· Contraindications: Avoid neuroleptics in patients with parkinsonism or Parkinson
· Precautions: Neuroleptics may cause extrapyramidal effects, and benzodiazepines
may lead to sedation. Both increase the risk of falls.

Follow up

Admission Criteria
New delirium is a medical emergency and requires admission except in the setting of
palliative home care

Discharge Criteria
· Resolution of precipitating factor(s)
· Safe discharge site if still delirious

Issues for Referral

· If delirium at discharge, will usually be followed in post-acute facility
· If no delirium at discharge, follow-up with primary care physician in 1-2 weeks

Usually improves with treatment of underlying condition, but may become chronic.

· Falls
· Pressure ulcers
· Malnutrition
· Functional decline
· Versedation
· Polypharmacy

Patient Monitoring
· Evaluate and assess mental status daily.
· Other depends on specific conditions present.

Falls are a major problem for elderly people, especially women. Some 30% of
community-dwelling elderly individuals fall each year, and the proportion increases
with age. Nonetheless, falling must not be viewed as accidental, inevitable, or


Falls are the most common cause of injury in patients over 65 years of age. Fifty
percent of elderly persons who fall do so repeatedly.


Balance and ambulation require a complex interplay of cognitive, sensory,

neuromuscular, and cardiovascular function and the ability to adapt rapidly to an
environmental challenge. With age, balance becomes impaired and sway increases.
The resulting vulnerability predisposes the older person to fall when challenged by
an additional insult to any of these systems. Thus, a seemingly minor fall may be due
to a serious problem, such as pneumonia or a myocardial infarction.

Much more commonly, however, falls are due to the complex interaction between a
variably impaired patient and an environmental challenge. While a warped floorboard
may pose little problem for a vigorous, unmedicated, alert person, it may be sufficient
to precipitate a fall and hip fracture in the patient with impaired vision, strength,
balance, or cognition. Thus, falls in older people are rarely due to a single cause, and
effective prevention entails a comprehensive assessment of the patient's intrinsic
deficits (usually diseases and medications), the routine activities, and the
environmental obstacles.

Intrinsic deficits are those that impair sensory input, judgment, blood pressure
regulation, reaction time, and balance and gait. Medications and alcohol use are
among the most common, significant, and reversible causes of falling. Other
treatable contributors include postprandial hypotension (which peaks 30 to 60 min
after a meal), insomnia, urinary urgency, foot problems, and peripheral edema [which
can burden impaired leg strength and gait with an additional 2 to 5 kg (5 to 10 lb)].
Since most falls occur in or around the home, a visit by a visiting nurse, physical
therapist, or physician often reaps substantial dividends.


Most individuals who fall will do so on a level surface and most will suffer an isolated
orthopedic injury. Falls are reported as the underlying cause of 9500 deaths each
year in patients older than age of 65 years. Many falls in the elderly population occur
in residential institutions such as nursing homes. In the >85-year-old age group, 20
percent of fatal falls occur in nursing homes.

There are age-related changes in postural stability, balance, motor strength,

coordination, and reaction time that make the elderly more prone to tripping and
falling, and may explain the increased incidence of falls. Also, decreased visual
acuity and increased memory loss can cause the patient difficulty in recognizing and
avoiding environmental hazards. Acute, preexisting, and chronic diseases also may
lead to falls. Syncope has been implicated in many cases of elderly patients who fall
and this may be secondary to dysrhythmias, venous pooling, autonomic
derangement, hypoxia, anemia, or hypoglycemia. Other contributing factors include
alcohol and medications, most notably sedative, antihypertensive, antidepressant,
diuretic, and hypoglycemic agents.

Falls are not a normal part of aging. A fall is a symptom, and emergency physicians
need to assess both the cause and the consequences of the fall. The causes of a fall
may include acute or chronic diseases, medications, and environmental factors.

Consequences of a fall include injury and fear of falling, resulting in a decrease in

activities. A fall can represent a sentinel event in an older person's life and result in a
downward spiral of decreased activities, leading to death.

As many as 50 percent of older patients admitted to the hospital after a fall die within
1 year. An emergency physician should obtain the history of what caused the fall and
determine whether further ED screening tests (electrocardiography, computed
tomography, laboratory tests, social service consultation, etc.) need to be done to
evaluate the cause. The patient should then be informed about fall assessment
programs that decrease the incidence and morbidity from falls.
Complications of Falls and Treatment

One out of four people who fall suffers serious injury. About 5% of falls result in
fractures, and an equal proportion cause serious soft tissue damage. Falls are the
sixth leading cause of death for older people and a contributing factor in 40% of
admissions to nursing homes. Resultant hip problems and fear of falls are major
causes of loss of independence.

Subdural hematoma is a treatable but easily overlooked complication of falls that

must be considered in any elderly patient presenting with new neurologic signs,
including confusion alone, even in the absence of a headache. Dehydration,
electrolyte imbalance, pressure sores, rhabdomyolysis, and hypothermia may also
occur and endanger the patient's life following a fall.

The risk of falling is related to the number of contributory conditions. Because the
relationship is multiplicative rather than additive, however, even minor improvement
in a number of these factors will reduce