Acute Focal Neurological Signs,

Meningism and Encephalitis

By
Kuhanesan
 Focal Neurological Signs
• Definition
focal signs or focal CNS signs are perceptual or behavioral
impairments which are caused by lesions in a
particular area of the central nervous system

• These signs are interpreted by neurologists to mean

that a given disease process is focal rather than
diffuse.

• Focal disease processes include for example tumors or

infarctions; diffuse disease processes include
meningitis or encephalitis.
 Frontal lobe signs
Frontal lobe signs are focal neurological signs that may help to indicate a frontal lobe
lesion:
Related to precentral gyrus:
•monoparesis or hemiparesis depending on extent of damage
•focal motor seizures - either spreading with a Jacksonian march or rapid
generalisation to give tonic-clonic seizures; status epilepticus is not an uncommon
presentation of frontal lobe tumours

Related to Broca's area:

•expressive/Broca's dysphasia if in dominant hemisphere

Related to supplementary motor area:

•paralysis of head and eye movements to opposite side - head and eyes deviated
towards side of lesion
 Frontal lobe signs
Related to prefrontal area:
•change in personality - inappropriate jocularity, loss of initiative and concern, akinetic mutism,
disinhibition, general retardation
•primitive reflexes - grasp, pout, palmar-mental, brisk jaw-jerk; changes in deep tendon reflexes
contralaterally
•unsteadiness in walking; rarely, gait apraxia
•resistance to passive movements of the limbs – paratonia

Related to paracentral lobule:

•incontinence of urine or faeces - cortical disinhibition

Orbital surface:
•unilateral or bilateral anosmia

A patient with a frontal lobe space-occupying lesion on one side may cause optic atrophy in one
eye, due to compression of the optic nerve, and papilloedema in the other eye, due to
secondarily raised intracranial pressure - Foster Kennedy syndrome.
Hemiplegic Gait This girl has a right
hemiparesis. Note how she holds
her right upper extremity flexed at
the elbow and the hand with the
thumb tucked under the closed
fingers (this is "cortical fisting").
There is circumduction of the right
lower extremity.
 Parietal Lobe Signs
The parietal lobe is the principal sensory area of the cerebral cortex. The manifestations of
damage may be specific to the dominant or non-dominant hemisphere, or it may be general:

Disease of either dominant or non-dominant hemisphere post-central gyral sensory cortex

produces contralateral disturbance of cortical sensation:
•impairment of postural sensation and sensation of passive movement (proprioception)
•impairment of tactile sensation - accurate localisation of light touch, two point discrimination
•sensory and visual inattention
•loss of ability to find a defined place (geographical agnosia)
•loss of ability to identify objects based on touch (astereognosia.)

Dominant hemisphere lesions:

•involving Wernicke's speech area - receptive dysphasia
•Gerstmann's syndrome
•loss of ability to read, write or calculate (dyslexia, dysgraphia, dyscalculia)
 Parietal Lobe Signs
Non-dominant lesions:
•neglect of contralateral limb, even if densely hemiplegic
•denial of weakness - anosognosia
•spatial neglect
•disappreciation of three dimensional sense - dressing dyspraxia, constructional
dyspraxia
•geographical agnosia - e.g. unable to find defined places

Involving the optic radiation deep in the parietal lobe:

•lower homonymous quadrantanopia
 Temporal Lobe Signs
The features of temporal lobe lesions are often slight.

Involving the auditory cortex:

•deafness without damage to the structures of the ear, described as cortical deafness,
may be complete if the lesion is bilateral - rare
•involving the surrounding association areas:
• in the dominant hemisphere - Wernicke's aphasia (loss of ability to
comprehend music or language, described as a sensory aphasia)
• in the non-dominant hemisphere - amusia
•tinnitus, auditory hallucinations
•temporal lobe epilepsy - complex partial seizure in the temporal lobes

Involving the middle and inferior temporal gyri:

•disturbance of memory and learning - deja vu, jamais vu, post-ictal amnesia
 Temporal Lobe Signs
Involving the limbic lobe:
•aggressive or antisocial behaviour
•inability to acquire new memories
•olfactory hallucinations, e.g. burning rubber

Involving the optic radiation:

•upper homonymous quadrantanopia

Temporal Lobe Epilepsy

 Occipital Lobe Signs
Usually involve visual sensation, and may include:
•total loss of vision (cortical blindness)

•loss of vision with denial of the loss (Anton's syndrome)

•loss of vision on one side of the visual field of both eyes (homonymous hemianopsia)

•visual agnosias, i.e. inability to recognize familiar objects, colors, or faces

•visual illusions such as micropsia (objects appear smaller) and macropsia (objects appear
larger)

•visual hallucinations, displaying elementary forms, such as zig-zags and flashes, in one half
of the visual field only for each eye. (In contrast, temporal lobe visual hallucinations display
complex forms, and fill the entire visual field.)
 Limbic Signs
Damage to the Limbic System involves loss or damage to memory, and may
include:

•Loss or confusion of long-term memory prior to focal neuropathy (Retrograde

amnesia)

•Inability to form new memories (Anterograde amnesia)

•Loss or reduced emotions (Apathy).

•Loss of olfactory fuctions.

•Loss of decision making ability.

 Cerebellar Signs
Usually involve balance and coordination, and may include:

•unsteady and clumsy motion of the limbs or torso (ataxia)

•inability to coordinate fine motor activities (intention tremor), e.g. "past-

pointing" (pointing beyond the finger in the finger-nose test)

•inability to perform rapid alternating movements (dysdiadochokinesis), e.g.

inability to rapidly flip the hands

•involuntary left-right eye movements (nystagmus)

Brainstem signs can involve a host of specific
sensory and motor abnormalities, depending on
which fiber tracts and cranial nerve nuclei are
affected.

Spinal cord signs generally involve unilateral

paralysis with contralateral loss of pain
sensation
 CRANIAL NERVES: SUMMARY TABLE.
Cranial nerve Nucleus name Nucleus Function Symptom/sign of damage
location

Olfactory (CNI) Anterior olfactory Olfactory tract Smell Anosmia

Optic (CNII) Lateral geniculate Thalamus Vision Blindness

nucleus

Oculomotor (CNIII) Oculomotor Midbrain Eye movement Eye deviates down & out

Edinger Westphal Midbrain (elevation, adduction) Loss of pupillary/accommodation reflexes

Trochlear (CNIV) Trochlear Midbrain Eye movement Diplopia, lateral deviation of eye

(depression of adducted eye)

Trigeminal (CNV) Principal Pons Facial sensation Facial aneasthesia

Spinal Medulla Mastication Loss of pain sensation

Mesencephalic Pons/midbrain Insignificant

Motor Pons Weakness/loss of mastication

Abducent (CNVI) Abducent Pons Eye movement (Abduction) Medial eye deviation

Facial (CNVII) Motor Pons Facial expresssion Paralysis of facial nerve muscles (+ hyperacuisis)

Solitary Pons Taste Loss of taste (anterior 2/3rds of tongue)

Superior salivatory Pons Salivation, lacrimation Dry mouth, loss of lacrimation

Vestibulocochlear (CN Vestibular Medulla Balance Vertigo, dysequilibrium, nystagmus

VIII)
Cochlear Medulla Hearing Hearing

Glossopharyngeal (CN Nucleus ambiguus Medulla Taste Loss of taste (posterior 1/3rd of tongue)
IX)
Inferior salivatory Medulla Salivation Insignificant

Solitary Medulla Innervation of pharynx Loss of gag reflex

Vagus (X) Nucleus ambiguus Medulla Swallowing & talking Dysphagia & hoarseness of voice

Dorsal motor Medulla Cardiac, GI tract, respiration Insignificant

vagal
Medulla Taste Loss of cough reflex (larynx/pharynx), loss of taste (hard
Solitary palate)

Cranial Accessory (XI) Nucleus ambiguus Medulla Pharynx/larynx muscles Insignificant

Spinal accessory Spinal accessory Cervical cord Neck & shoulder movement Head turning/shoulder shrugging weakness

Hypoglossal (XII) Hypoglossal Medulla Tongue movement Atrophy of tongue muscles, deviation on protrusion,
fasciculaations
 Meningism
• Meningism is the triad of nuchal rigidity (neck stiffness), photophobia
(intolerance of bright light) and headache.

• It is a sign of irritation of the meninges, such as seen in meningitis,

subarachnoid hemorrhages and various other diseases.

• "Meningismus" is the term used when the above listed symptoms are
present without actual infection or inflammation; usually it is seen in
concordance with other acute illnesses in the pediatric population.

• Related clinical signs include Kernig's sign and three signs all named
Brudzinski's sign.
 Meningism
The main clinical signs that indicate meningism are nuchal rigidity, Kernig's
sign and Brudzinski's signs. None of the signs are particularly sensitive.

•Nuchal rigidity is the inability to flex the head forward due to rigidity of the
neck muscles; if flexion of the neck is painful but full range of motion is
present, nuchal rigidity is absent.

•Kernig's sign (after Waldemar Kernig (1840-1917), a Baltic German

neurologist) is positive when the leg is bent at the hip and knee at 90 degree
angles, and subsequent further extension in the knee is painful (leading to
resistance). This may indicate subarachnoid haemorrhage or meningitis.
Patients may also show opisthotonus—spasm of the whole body that leads to
legs and head being bent back and body bowed backwards.
• Jozef Brudzinski (1874-1917), a Polish pediatrician, is credited with
several signs in meningitis. The most commonly used sign (Brudzinski's
neck sign) is the appearance of involuntary lifting of the legs in meningeal
irritation when lifting a patient's head off the examining couch, with the
patient lying supine. Other signs attributed to Brudzinski:

• The symphyseal sign, in which pressure on the pubic symphysis leads to

abduction of the leg and reflexive hip and knee flexion.

• The cheek sign, in which pressure on the cheek below the zygoma leads
to rising and flexion in the forearm.

• Brudzinski's reflex, in which passive flexion of one knee into the abdomen
leads to involuntary flexion in the opposite leg, and stretching of a limb
that was flexed leads to contralateral extension
Meningism signs
 Encephalitis
Introduction
•Encephalitis is an acute infection and inflammation of the brain itself. This is in contrast to meningitis,
which is an inflammation of the layers covering the brain.

•Encephalitis is generally a viral illness. Viruses such as those responsible for causing cold sores,
mumps, measles, and chickenpox can also cause encephalitis. A certain family of viruses, the
Arboviruses are spread by insects such as mosquitoes and ticks. The equine (meaning horse), West Nile,
Japanese, La Crosse, and St. Louis encephalitis viruses are all mosquito-borne. Although viruses are the
most common source of infection, bacteria, fungi, and parasites can also be responsible.

•The illness resembles the flu and usually lasts for 2-3 weeks. It can vary from mild to life-threatening,
and even cause death. Most people with a mild case can recover fully. Those with a more severe case
can recover although they may have damage to their nervous system. This damage can be permanent.

•Japanese encephalitis virus is the most common arbovirus in the world (virus transmitted by blood-
sucking mosquitoes or ticks) and is responsible for 50,000 cases and 15,000 deaths per year. Most of
China, Southeast Asia, and the Indian subcontinent are affected.
 Encephalitis
Causes

Viral
•Viral encephalitis can be due either to the direct effects of an acute infection, or as one of
the sequelae of a latent infection. Usually cause by arboviruses spread by mosquitoes and
ticks. A common cause of encephalitis in humans is herpes (HSE) which may cause
inflammation of the brain.

Bacterial and other

•It can be caused by a bacterial infection such as bacterial meningitis spreading directly to the
brain (primary encephalitis), or may be a complication of a current infectious disease syphilis
(secondary encephalitis). Certain parasitic or protozoan infestations, such as toxoplasmosis,
malaria, or primary amoebic meningoencephalitis, can also cause encephalitis in people with
compromised immune systems. Lyme disease and/or Bartonella henselae may also cause
encephalitis.
•Another cause is granulomatous amoebic encephalitis.
 Encephalitis
Diagnosis
•Patients with encephalitis present with acute onset of fever, headache, confusion, and
sometimes seizures. Younger children or infants may present irritability, poor appetite and
fever.

•The signs and symptoms of encephalitis are the same for adults and children. Signs and
symptoms may last for 2-3 weeks, are flu-like, and can include 1 or more of the following :
Fever, Fatigue, Sore throat, Stiff neck and back, Vomiting, Headache, Confusion, Irritability,
Unsteady gait, Drowsiness, Visual sensitivity to light

•More severe cases may involve these signs and symptoms: Seizures, Muscle weakness,
Paralysis, Memory loss, Sudden impaired judgment, Poor responsiveness

•Neurological examinations usually reveal a drowsy or confused patient. Stiff neck, due to the
irritation of the meninges covering the brain, indicates that the patient has either meningitis
or meningoncephalitis.
 Encephalitis
• CT scan often is not helpful, as cerebral abscess is uncommon. Cerebral abscess is more
common in patients with meningitis than encephalitis. Bleeding is also uncommon except in
patients with herpes simplex type 1 encephalitis. Magnetic resonance imaging offers better
resolution.

• In patients with herpes simplex encephalitis, electroencephalograph may show sharp waves
in one or both of the temporal lobes.

• Lumbar puncture procedure is performed only after the possibility of prominent brain
swelling is excluded by a CT scan examination. Examination of the cerebrospinal fluid obtained
by a lumbar puncture procedure usually reveals increased amounts of protein and white
blood cells with normal glucose, though in a significant percentage of patients, the
cerebrospinal fluid may be normal.

• Diagnosis is often made with detection of antibodies in the cerebrospinal fluid against a
specific viral agent (such as herpes simplex virus) or by polymerase chain reaction that
amplifies the RNA or DNA of the virus responsible (such as varicella zoster virus).
 Encephalitis
Treatment
•Encephalitis is usually a viral illness, which means that antibiotics are not used to treat it. The only available
vaccine for prevention is for Japanese encephalitis.

•Treatment is usually symptomatic. People with encephalitis are kept hydrated with IV fluids while monitoring for
brain swelling.

•Herpes encephalitis can cause rapid death if not diagnosed and treated promptly. Therefore, medication is usually
started when the doctor suspects herpes to be the diagnosis without waiting for the confirmatory results.

•Reliably tested specific antiviral agents are available only for a few viral agents (e.g. acyclovir for herpes simplex
virus) and are used with limited success for most infection except herpes simplex encephalitis.

•In patients who are very sick, supportive treatment, such as mechanical ventilation, is equally important.

•Corticosteroids (e.g. methylprednisolone) are used to reduce brain swelling and inflammation.

•Sedatives may be needed for irritability or restlessness.

•Anticonvulsants are used to prevent seizures.

Japanese Encephalitis
Transmission Cycle

Neurological changes
seen in Encephalitis