CNS about:srcdoc

CNS
This is characterised by unilateral lancinating facial
pain, most commonly involving the second and/or
What is trigeminal neuralgia
third divisions of the trigeminal nerve territory,
usually in patients over the age of 50 years.

Pain: repetitive, severe and very bried

(seconds or less)
Pain triggered by: touch, cold wind or eating
Physical signs usually absent
Spasms may make patient wince and sit
Clinical features of trigeminal neuralgia
silently (tic douloureux)
Tendency for condition to remit and relapse
over many years
Rarely: trigeminal neuralgia + cluster
headaches = cluster-tic

Pain responds to carbamazepine(upto 1200

mg/day) (start with low dose and increase
gradually, according to effect)
Patient unable to tolerate carbamazepine:
oxcarbazepine, gabapentin (upto 2400 mg/
day), pregabalin, amitriptyline or
glucocorticoids may be used
Management of trigeminal neuralgia Decompression of vascular loop
encroaching on trigeminal root may be
performed if pharmacological therapy is
uneffective
Localised injection of alcohol or phenol into
peripheral branch of nerve may be effective
Radiofrequency thermal rhizo-tomy
Gamma radiosurgery

CT and MRI to detect underlying cause

Investigations for trigeminal neuralgia High resolution MR angiography can be
used to visualize aberrant vessels

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Typically seen in middle-aged depressed

females
Pain: constant and of burning type, centered
on maxilla but may spread to rest of face on
affected side
What is atypical facial pain Sometimes it may involve other side of face,
neck or back oof head
Treatment: tricyclic antidepressants,
analgesics, carbamazepine or phenytoin
may be tried
Response to therapy is poor

Similar in quality to trigeminal neuralgia but

is less common
Site of pain: one side of throat in area of
tonisllar fossa and may radiate to ear (it may
also be localised in the ear)
Initiation of pain: swallowing, coughing,
chewing or yawning
What is glossopharyngeal neuralgia Pain may be accompanied with syncope
Sensory and motor exam is normal
No cause is typically demonstrable (some
cases = multiple sclerosis)
Treatment: same as trigeminal neuralgia
(carbamazepine, microvascular
decompression and partial rhizotomy (latter
2 in refractory cases))

More common in elderly when 1st division

of CN III is involved
Pain: continuous, burning and throughout
affected teritory of the nerve
Pain may last for years
What is post-herpetic neuralgia
Treatment: simple analgesics, phenytoin
(300 mg/day), carbamazepine (upto 1200
mg/day), gabapentin (upto 3200 mg/day).
Tricyclic agents alone or with phenothiazine
may be tried in severe cases

Clinical features of migraine Prodrome of malaise, irritability or

behavioural change for some hours or days
Some patients report an aura: may manifest
as any neurological symptom but is most

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often visual, consisting of fortification

spectra (shimmering, silvery zig zag lines
marching across visual fields) for upto 40
mins. May leave a trail of temporary visual
field loss (scotoma)
Sensory symptoms of aura characteristically
spread over 20-30 mins from one part of
body to another
Motor and language function may also be
affected in aura
Aura need not always precede a migrane
and in some patients aura may persist
beyond migraine episode
Migraine headache: severe and throbbing
with photophobia, phonophobia and
vomitting lasting from 4-72 hrs
Movement worsens pain

Management of migraine Avoidance of

identified triggers or
exacerbating factors
Acute attack:
Simple analgesia with
aspirin, paracetamol
or NSAIDs and may
be combines with
dopamine
antagonists
(metoclopramide,
domperidone, etc)
Rest in quiet, dark
room
Severe attacks can be
aborted by use of 5-
HT agonists
(sumatriptan 6 mg SC
repeated at 1 hr with
no more than 2
doses/day or 25-100
mg orally repeated at
2 hrs to maximum of
200 mg/day)
administered orally,
subcutaneously or
nasally

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Ergotamine (1-2 mg
orally repeated every
30 mins to maximum
of 10 mg/day or 16
mg/week)
preparations may
lead to dependence.
May be combined
with caffeine
Overuse of meds =
medication overuse
headache
Frequent attacks (more than 3/
month): prohylactic therapy
Vasoactive drugs such
as beta blockers and
ACEI or ARBs
Antidepressants
(amitriptyline,
dosulepin)
Antiepileptics
(topiramate): may be
teratogenic
Refractory migraine:
monoclonal
antibodies to
calcitonin gene-
related peptide
receptors
Women with aura
should avoid
oestrogen treatment
or HRT

Classical: headache associated with aura

Common: headache w/o aura
Migraine equivalent: focal neurological
Types of migraine
deficit w/o headache
Complicated: transient focal neurological
features or persistent neurological deficits

Variants of migraine Basilar: vertigo, diplopia, and dysarthia

followed by headache and impaired
sensorium. Transient blindness may occur
(typically in young females)

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Ophthalmic: pain around eye, nausea,

vomitting and diplopia (due to transient
external ophthalmoplegia mainly involving
CN III and rarely VI)
Facial (carotidynia, lower half headache):
pain occurs repeatedly in jaw, neck and
periorbital area, accompanied with
tenderness and prominent pulsations of
cervical carotid artery (soft tissue swelling
may be present over artery). May be
associated with throbbing headache.
Common in older patients and precipitated
by dental trauma

Classify seizures

Awareness may become impaired if spread

occurs to temporal lobes
Patients stop and stare blankly, often
blinking repetitively, making smacking
movements of their lips or displaying other
automatisms
Consciouness returns after a few minutes,
but patient may be muddled or drowsy for
Clinical features of focal seizures
upto an hour
Seizures arising from anterior parts of
frontal lobe may produce bizarre behaviour
patterns (limb posturing, sleep walking or
frenetic, ill-directed motor activity with
incoherent screaming (video EEG may be
needed to differentiate from psychogenic
attacks)

Causes of focal seizures

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Clinical features of generalised seizures Tonic-clonic seizures:

Inital aura may be present (depending on
cortical area from which seizure originates)
Patient becomes rigid (tonic) and
unconscious, falling heavily if standing up
(like a log) and risking facial injury.
During this phase: breathing stops and
central cyanosis may occur
As cortical discharges reduce in frequency,
jerking (clonic) movements emerge for 2
mins, followed by a flaccid state of deep
coma and patient regaining awareness
(though they may be confused, disoriented
and/or amnesic)
Urinary incontinence and tongue biting may
occur
Patient usually feels sleepy and unwell
Sequelae: headache or myalgia
Absence seizures
Prev: petit mal
Start in childhood and are mistaken for focal
seizures due to brevity
Occur frequently (20-30 times/day) =
mistaken for daydreaming/poor
concentration
Myoclonic seizures:
Brief, jerking movements, predominating in
the arms
More marked in morning or on awakening
from sleep
Provoked by fatigue, alcohol, sleep
deprivation
Atonic seizures:
Involve brief loss of muscle tone, resulting in
heavy falls w/ or w/o loss of consciousness
Occur only in the context of epilepsy
syndromes
Tonic seizures:
Generalised increase in tone and associated

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loss of awareness
Usually part of epilepsy syndrome
Clonic seizures:
Similar to tonic-clonic, w/o tonic phase

Epileptic spasms
Unusual in adults; seen in infants
Signify widespread cortical disturbance
What are seizures of uncertain generalised
or focal nature Marked contractions of axial musculature,
lasting fraction of a second and recurring in
clusters of 5-50
Often on awakening

Causes of tonic-clonic seizures

All patients with transient loss of

consciousness should have 12-lead ECG
Suspected/definite seizure: cranial imaging
via MRI or CT (low yield unless focal signs
Investigations to be done for single seizure are present)
EEG may aid prognosis once firm diagnosis
has been made
Investigations for infective, toxic or
metabolic cause may be needed

Investigations to be done for epilepsy EEG aids in

establishing type of
epilepsy and guides
treatment
Inter-ictal EEG is
abnormal in ½ of
patients with
recurrent seizures
(hence can’t be used
to exclude epilepsy)
Ambulatory EEG

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recording or video
EEG monitorring may
aid in differential
diagnosis
Imaging
Indications: epilepsy
started post age 16
years, seizure has
focal features
clinically, EEG shows
focal seizure souce
and control of seizure
is difficult or
deteriorating
Cannot establish
diagnosis but can
identify cause
MRI needed to
demonstrate subtle
changes
(hippocampal
sclerosis)

List some common generalised epilepsy

syndromes

Electroclinical epilepsy syndromes

Management of epilepsy Immediate care:

Little can or needs to
be done during
convulsive seizure
First aid and common
sense maoeuvres to
limit damage or
seconday
complications

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Ensure nothing is
inserted into patient’s
mouth
Lifestyle advice
Antiepileptics:
Consider when risk of
recurrence is high
Focal epilepsies:
Iamotrigine best
tolerated
monotherapy
Unclassified or
genetic epilepsies:
Valproate
Blood levels need to
be interpreted
carefully and dose
changes made to
treat the patient
rather than to bring a
serum level into the
‘therapeutic range’.
Withdrawl of
medication may be
considered after
patient has been
seizure free for more
than 2 years and
should be done
slowly over weeks or
months (recurrence is
possible)
Surgery:
For patients with drug
resistant epilepsy or
those who continue
to experience seizures
despite therapy
Involves surgical
resection of
epileptogenic brain
tissue
Less invasive
treatments: vagal
nerve stimulation or

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deep brain
stimulation

Seizure activity not resolving spontaneously

or recurrent seizure with no recovery of
consciousness in between
Diagnosis is clinical
What is status epilepticus Prolonged seizure activity: movements may
become more subtle, cyanosis, pyrexia,
acidosis and sweating may occur
Complications: aspiration, hypotension,
cardiac arrhythmias and renal/hepatic failure

Management of status epilepticus

Loss of facial expression at side of palsy

Furrows of forehead are absent
Eyelids do not close completely on affected
side (on attempted closure, eyeball on
affected side rolls up = Bell’s phenomenon)
Drooping of corner of mouth and dribbling
Clinical features of facial nerve palsy
of saliva
Loss of nasiolabial fold
Collection of food b/w teeth and lips
Inability to whistle or blow
Hyperacusis if nerve to stapedius is
damaged

Causes of facial nerve palsy Supranuclear:

cerebral thombosis,
cerebral embolism
and brain tumour
Melkersson-Rosenthal
syndrome: recurrent
facial nerve palsy +
recurrent facial
edema + plicated

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tongue
Ramsay Hunt
syndrome: herpes
zoster complication
Facial diplegia:
bilateral infranuclear
palsy seen in Guillain-
Barre syndrome and
sarcoidosis

Compare supranuclear and infranuclear

facial palsy

Lesion outside stylomastoid foramen: only

moto manifestations are present. Taste is
unaffected and there is no hyperacusis
Lesion in facial canal: hyperacusis and loss
of taste. Other cranial nerves may be
involved if lesion is near internal auditatory
Localising the lesion: infranuclear facial meatus
palsy Pontine lesion: CN VI may also be involved
and there is hemiplagia of opposite side
(crossed hemiplagia)
If recovery of motor function is incomplete:
synkinesis
Crocodile tears
Jaw winking

Results from damage of corticonuclear

fibers from motor cortex to facial nucleus
Upper part of face involved to lesser extent
(as it is innervated by both motor cotices
unlike lower part of face is innervated by
Localising the lesion: supranuclear facial opposite hemisphere only)
palsy
Paralysis of arm and leg or same side or
apahsia
Taste sensation not involved
Emotional facial movements preserved
Lesion is on opposite side of palsy

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Type of idiopathic infranuclear facial palsy. Associated

What is Bell’s palsy
with reactivation of herpes simplex type 1 infection

Abrupt onset or subacute

Max weakness within 48 hrs
Pain around ear prior to weakness
Motor manifestations same as other LMN
facial palsies
Clinical features of Bell’s palsy
Bell’s phenomenon present
Loss of taste in anterior 2/3rd of tongue on
same side
Hyperacusis if nerve to stapedius is involved
Diminished salivation and tear secretion

MRI: may show swelling and enlargment of

Investigations to be done for Bell’s palsy geniculate ganglion and facial nerve
EMG has prognostic value

Symptomatic:
Massage facial msucles
Protection of eye during sleep to prevent
corneal damage, use of lubricating eye
drops
Treatment of Bell’s palsy
Specific:
Administer glucocorticoids w/ or w/o
acyclovir (prednisolone 60-80 mg daily for 5
days and then tapered over next 5 days)
Acyclovir: 400 mg 5 times daily for 10 days

Acute purulent: pyogenic, septic and

bacterial
Classify meningitis
Viral: aseptic
Chronic: tuberculous, fungal

List some organisms causing acute

bacterial meningitis

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Classical triad: fever,

headache and neck
rigidity (increased
resistance to passive
flexion of neck)
Kernig’s sign (passive
extension of knee
causes pain and
spasm of hamstrings)
Brudzinski’s sign:
passive flexion of
neck results in
spontaneous flexion
of hips and knewws
Impairment in
Clinical features of acute bacterial sensorium
meningitis Nausea, vomitting,
photophobia
Rash and
adrenocortical failure
with shock
(Waterhouse
Friderichsen
syndrome
Seizures and raised
ICP
Complications:
sensorineural hearing
loss, decreased
intellectual function,
seizure and gait
disturbances

Investigations to be done for bacterial Lumbar puncture and

meningitis CSF exam: check
pressure, cell count,
protein, glucose,
smear stain for
bacteria and culture.
PCR if necessary
CT scan: to rule out
presence of
intracranial space-
occupying lesion
prior to lumbar

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puncture
Blood examination:
leukocytosis and
blood culture

Empirical therapy to
be started prior to
CSF exam:
ceftriaxone,
vancomycin and
ampicilin (esp in
patients less than 3
months or greater
than 55 years in age
as well as
immunocompromised
patients)
Adjunctive therapy
with dexamethasone
(10 mg given 15-20
mins before or
Treatment of bacterial meningitis concurrent with 1st
dose of antibiotic
every 6hrs for 4 days)
Supportive therapy:
patients with raised
ICP are managed in
ICU. IV mannitol and
elevation of patients
head to 30 degrees is
recommended
Prevention:
prophylactic therapy
with oral rifampicin
for 2 days or single
dose of ciprofloxacin,
azithromycin or IM
ceftriaxone

Most common viruses involved in viral Enteroviruses: coxsackie, echo, polio virus
meningitis Mumps
Measles
Influenza
Herpes zoster
Herpes simplex

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HIV
EBV
Hepatitis

Headache
Neck rigidity
Kernig’s and Brudzinski’s signs absent
Seizures and focal neural deficit absent
Clinical features of viral meningitis Mildly altered sensorium
Fever, myalgia, malaise, anorexia, vomitting,
abdominal pain
CSF: lymphocytosis, slightly increased
protein and normal sugar

Usually supportive
Treatment of viral meningitis Acyclovir may be used
Benign and self-limiting

Insidious or acute onset

Headache
Vomiting
Low grade fever
Cranial nerve palsies
Clinical features of tuberculous meningitis
Papilledema
Focal neurological deficit
Complication: hydrocephalus
Treatment is anti-tubercular with addition of
steroids

CSF exam: fluid is straw colored clear but

when allowed to stand fine clot (spider web)
is formed, high lymphocyte count, high
Investigations to be done for tuberculous protein and high glucose. Acute cases:
meningitis polymophs predominate. Positve AFB
culture
CT or MRI: meningeal enhancement or
hydrocephalus

What is fungal meningitis Seen in the immunocompromised

Findings similar to tuberculous meningitis
Diagnosis confirmed via microscopy: india
ink preparation for cryptococcus

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Treatment: amphotericin B followed by oral

fluconazole

History of trauma
Ingestion of drugs or toxins
Presence of chronic disease of liver, kidneys,
History of comatose patient
heart or lungs
DM
Circumstances preceding symptoms

Presence of fever: systemic infection,

meningitis, etc
Hypothermia: alcoholism, barbiturate
poisoning, hypothyroidism, hypoglycemia
and circulatory failure
General physical exam of comatose patient
Severe hypertension: hypertensive
encephalopathy or cerebral hemorrhage
Hypotension: sepsis, HF, internal
hemorrahge, alcoholism, barbiturate
poisoning

Neurological exam of comatose patient Level of

consciousness
assessed by Glasgow
scale
Hemiplagia: stroke
Myoclonus: metabolic
encephalopathy, drug
intoxication
Decorticate rigidity:
lesion rostral to
midbrain
Decerebrate rigidity:
lesion in brain or
caudal diencephalan
Unilaterally dilated
pupils: CN III damage
Bilaterally dilated
pupils: severe
midbrain lesion,
atropine or methyl
alcohol intoxication
and severe anoxic
encephalopathy

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Bilaterally small or pin

point pupils: narcotic
overdose, metabolic
encephalopathy and
thalamic/pontine
lesions
Conjugate horizontal
deviation of eye ball
on one side: damage
to pons on other side
or frontal lobe lesion
of same side
Eyes turned down
and inwards:
midbrain lesion
Dolls eye
phenomenon: intact
brain stem
oculomotor function
Caloric stimulation
test: loss of reflex
indicates brain stem
damage
Cheyne stokes
breathing: bilateral
hemispheric damage
Kussmaul’s breathing:
metabolic acidosis
Presence of
herniatiation

CBC
Blood sugar, urea
Serum sodium, potassium and calcium
LFT
Investigations to be done for comatose
Serum ammonia, ethanol
patient
TFT
CT and MRI
CSF exam
EEG

Management of comatose patient General:

Maintain ABCs
Maintain normal body temp

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Administic O2
Mechanical ventilation
Medication:
IV thiamine 100 mg
Dextrose 50 ml (50%)
Rapid correction of cause
IV naloxone: opiate intoxication
Flumazenil: benzodiapine intoxication
IV antibiotics: meningitis, septicaemia
Manage ICP: IV mannitol, hyperventilation
and dexamethason
Operative:
Surgical eval of hematoma or hemorrhage
Shunt for hydrocephalus
Surgery for structural lesion

A state of cessation of cerebral function while

somatic function is maintained by artificial means and
the heart continues to pump.
Essential elements for diganosis:
Widespread cortical destruction reflected by
deep coma and unresponsiveness to all
stimuli including visual, auditory or painful
stimuli. There is no spontaneous movement
or any motor response to noxious stimuli.

What is brain death Brain stem damage shown by absence of

papillary response, loss of oculo-vestibular,
corneal or gag reflexes
Destruction of medulla manifested by
complete apnoea
Other diagnostic tests:
EEG
Radionuclide brain scan
Somato-sensory-evoked pontentials
Convential angiography

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