Neurology 135

MEDICINE AND ALLIED

NEUROLOGY
 Neurology 137

Chapter 1
HEADACHE
Manoj S, S K Sharma
1

Headache can be quite debilitating, although most TENSION TYPE HEADACHE

MEDICINE AND ALLIED

headaches are not caused by life-threatening disorders.
Most headaches are caused by one of four syndromes: Symptoms — Symptoms of tension type headaches
(TTH) include:
• Tension-type headache
• Migraine headache • Pressure or tightness around both sides of the head
• Chronic daily headache or neck
• Cluster headache • Mild to moderate pain that is steady and does not
throb
CAUSES OF HEADACHE
• Pain is not worsened by activity
Primary headache syndromes • Pain can increase or decrease in severity over the
Migraine course of the headache
Tension headache • There may be tenderness in the muscles of the head,
Cluster headache neck, or shoulders
Benign paroxysmal headache
People with TTH often feel stress or tension before their
Secondary headache
headache. Unlike migraine, tension headaches occur
Intracranial causes without other symptoms such as nausea, vomiting,
Subdural and intracerebral hematoma sensitivity to lights and sounds, or an aura. However,
Subarachnoid hemorrhage some people have symptoms of both tension and
Brain abscess, meningitis, encephalitis migraine headache.
Obstructive hydrocephalus
Vasculitis MIGRAINE HEADACHE :
Benign intracranial hypertension (pseudotumor
cerebri) Recurrent headache disorder manifesting in attacks
Cerebral ischemia or infarction lasting 4-72 hours. Typical characteristics of the
headache are unilateral location, pulsating quality,
Extracranial causes
moderate or severe intensity, aggravation by routine
Giant cell arteritis (temporal arteritis)
physical activity and association with nausea and/or
Sinusitis
photophobia and phonophobia
Glaucoma
Optic neuritis Diagnostic criteria:
Dental diseases A. At least 5 attacks fulfilling
Temporomandibular joint disease criteria B-D
Disease of cervical spine B. Headache attacks lasting 4-72
Systemic causes hours (untreated or unsuccessfully treated)
Fever, hypoxia, hypercapnia, hypertension, C. Headache has at least two of
the following characteristics:
anemia, allergy
1. unilateral location
Drugs ( nitrates)
2. pulsating quality
Depression 3. moderate or severe
pain intensity
 138 Textbook of Family Medicine

4. aggravation by or • The headache is usually deep, excruciating,

causing avoidance of routine physical activity continuous, and explosive in quality, although
(eg, walking or climbing stairs) occasionally it may be pulsatile and throbbing.
D. During headache at least one • The attack may occur up to eight times per day but is
1 of the following:
1. nausea and/or vomiting
usually short in duration (between 15 minutes and
three hours).
2. photophobia and phonophobia • The pain typically begins in or around the eye or
E. Not attributed to another temple; less commonly it starts in the face, neck, ear,
or side of the head.
disorder
• The pain is always on one side.
MEDICINE AND ALLIED

Migraine without aura is the commonest subtype of
migraine. It has a higher average attack frequency and is
usually more disabling than Migraine with aura. The
aura is the complex of neurological symptoms that
occurs just before or at the onset of migraine
headache. Most patients with migraine have
exclusively attacks without aura. Many patients
who have frequent attacks with aura also have
attacks without aura Premonitory symptoms occur
hours to a day or two before a migraine attack
(with or without aura). They include various
combinations of fatigue, difficulty in concentrating,
neck stiffness, sensitivity to light or sound, nausea,
blurred vision, yawning and pallor.
Table 1: Drugs used for prophylactic therapy of
migraine
Drug Dosage (daily)
Propranolol 80-320 mg
Amitriptyline 10-50 mg (at night)
Sodium valproate 300-1000 mg
Cyproheptadine 4-16 mg
Methysergide 4-8 mg
Verapamil 80-240 mg
CLUSTER HEADACHE
Cluster headaches are severe, debilitating headaches that
occur repeatedly for weeks to months at a time, followed
by periods with no headache. Cluster headaches are
relatively uncommon, affecting less than one percent of
people. Men are affected more commonly than women,
with a peak age of onset of 25 to 50 years.
SYMPTOMS:
• Begin quickly without any warning and reach a peak
within a few minutes.
• Most people with cluster headache are restless and
may pace or rock back and forth when an attack is in
progress.
• Cluster headaches are associated with eye redness
and tear production on the side of the pain, a stuffy
and runny nose, sweating, and pale skin.
• Some people are light sensitive in the eye on the
affected side.
Cluster headaches can begin at any age. People with
cluster headaches are more likely to have family
members who also have cluster headaches. Drinking
alcohol can bring on a cluster headache.
CHRONIC DAILY HEADACHE
Some people develop very frequent headaches, as
frequent as every day in some cases. When a headache is
present for more than 15 days per month for at least three
months, it is described as a chronic daily headache.
Chronic daily headache is not a type of headache but a
category that includes frequent headaches of various
kinds. Most people with chronic daily headache have
migraine or tension-type headache as the underlying type
of headache. They often start out having an occasional
migraine or tension-type headache, but the headaches
became more frequent over months or years. Some
people with frequent headache use headache medications
too often, which can lead to medication-overuse
headaches.
Medication-overuse headache — Medication-overuse
headache (MOH) may occur in people who have
frequent migraine, cluster, or tension-type headaches,
which leads them to overuse pain medications. A vicious
cycle occurs whereby frequent headaches cause the
person to take medication frequently (often non-
prescription medication), which then causes a rebound
headache as the medication wears off, causing more
medication use, and so on.
 Neurology 139

Overuse of any number of pain medications can increase

the risk of developing medication-overuse headaches.

OTHER TYPES OF HEADACHE

There are a number of other causes of headache.

1
DANGER SIGNS
Sinus headache -
The vast majority of headaches are not life threatening.

MEDICINE AND ALLIED

Recurrent headaches related to sinus infections are
uncommon. Many, if not most, people diagnosed with
sinus headaches actually have migraine headaches
Sinus-related pain usually lasts for several days (unlike a
typical migraine) and does not cause nausea, vomiting,
or sensitivity to noise or light (as seen in migraine)
Post-trauma headaches -
Headaches that occur within one to two days after a head
injury are relatively common. Most people report a
generalized dull, aching, constant discomfort that
worsens intermittently. Other common symptoms include
vertigo (sensation of spinning), lightheadedness,
difficulty concentrating, problems with memory,
becoming tired quickly, and irritability.
Red flags are headaches that
• Comes on suddenly, becomes severe within a few
seconds or minutes, or that could be described as
"the worst headache of your life"
• Is severe and occurs with a fever or stiff neck
• Occurs with a seizure, personality changes,
confusion, or passing out
• Begins quickly after strenuous exercise or minor
injury
• Is new and occurs with weakness, numbness, or
difficulty seeing. While migraine headaches can
sometimes cause these symptoms, you should be
evaluated urgently the first time these symptoms
appear.
HEADACHE TREATMENT

Post-trauma headaches may continue for up to a few Commonly treated with NSAIDS, behavioral therapy and
months, although anyone with a headache that does not specific treatment in case of migraine and cluster
begin to improve within a week or two after a traumatic headaches.
event should be evaluated.

Approach to a Case of Headache

A detailed history is important in the case of headache.
The onset, severity and the site of headache are
important. Acute severe headache may suggest
subarachnoid hemorrhage or meningitis. Hemicranial
headache is a feature of migraine. Inquiry should be
made about precipitating factors like alcohol, emotional
stress, foods or medications. Chewing movements may
exacerbate the pain due to temporomandibular joint
disease, trigeminal neuralgia and glossopharyngeal
neuralgia. Cranial CT or MRI is indicated if the onset of
headache is new at middle age, progressive headache that
disturbs sleep, or is associated with neurological
symptoms or signs.
 140 Textbook of Family Medicine

Chapter 2
SEIZURES, EPILEPSY & STATUS EPILEPTICUS
1
Kamal K Salwani, S K Sharma, Neeta Bhargava

Seizure is a transient clinical event due to abnormal Degenerative

MEDICINE AND ALLIED

paroxysmal excessive discharges from a group of central Alzheimer’s disease

nervous system neurons. The seizure may present in Drugs
form of motor, sensory, autonomic or psychic manifes- Penicillins
tations.The motor form of seizure is called convulsion Theophylline
Chloroquine, Mefloquine
Epilepsy is defined as any disorder characterized by
Psychotropic agents
recurrent seizures due to chronic underlying
process. A single seizure is not epilepsy. Table 2: Classification of seizures
1. Partial seizures
Table 1: Causes of seizures Simple partial seizures
Complex partial seizures
Idiopathic Partial seizures with secondary generalization
Genetic 2. Primarily generalized seizures
Neurofibroma Absence (petit mal)
Inborn errors of metabolism Tonic clonic grand mal
Trauma Myoclonic
Birth trauma Tonic
Head injury Atonic
3. Unclassified seizures
Metabolic Infantile spasm
Alcohol withdrawal Neonatal seizures
Hypoglycemia 4. Status epilepticus
Hypocalcemia
Hyponatremia
Hypoxia PARTIAL SEIZURES
Renal failure
Liver failure Simple partial seizures are those where consciousness is
Intracranial space occupying lesions preserved whereas it is impaired in complex partial
Tuberculoma seizures. Partial seizures may spread diffusely
Neurocysticercosis throughout the cortex and result into secondary
Brain abscess generalized seizures. The manifestations depend on the
Brain tumor area of the brain involved and may be in the form of
Cerebrovascular diseases motor, sensory, autonomic or psychic symptoms.
Hemorrhage
Emboli Simple Partial Seizures
Infections Various presentations of simple partial seizures are;
Encephalitis
Meningitis a. Focal motor: The jerky movements of limbs or other
HIV
parts of the body depending upon the area of the
Toxoplasmosis
motor cortex involved.
Inflammatory
SLE b. Somatosensory: Localized paresthesias if sensory
Sarcoidois cortex is involved.

c. Special sensory: Involvement of visual, auditory,
olfactory and gustatory regions of the brain can lead
to light flashes, buzzing, unusual odor (burning
rubber) or epigastric sensations.
d. Autonomic: Flushing, sweating and piloerection are
due to autonomic involvement.
e. Psychic: Illusions, hallucinations, affective
disturbances and, déjà vu can be the manifestations
of simple partial seizures.
Complex Partial Seizures
Complex partial seizures arise generally from the
temporal or frontal lobes. These are focal seizure
activities accompanied with impaired consciousness. The
patient stares blankly (black outs) and has involuntary
automatic behavioral movements such as chewing, lip
smacking, emotion display or running (automatism).
The patients are drowsy following seizures and there is
amnesia about the recollection of ictal (seizure) phase.
Manifestations of simple partial seizure (aura) may
precede complex seizures and is the same (stereotypic)
every time in a particular patient.
PRIMARY GENERALIZED SEIZURES
Tonic-clonic Seizures
Tonic-clonic seizures (grand mal, primary generalized
seizures) may occur abruptly without warning or there
may be some premonitory symptoms. The presence of
aura suggests partial seizure with secondary
generalization. There is sudden loss of consciousness and
the patient may fall on the ground and sustain injuries.
The initial phase is characterized by increased muscle
tone throughout the body (tonic phase). Cyanosis,
impaired respiration, pooling of secretions in the oral
cavity occurs because of tonic contractions of muscles of
respiration. Increased tone in laryngeal muscles may
cause ‘ictal cry’. Tongue bite may occur due to
contraction of jaw muscles. Increased sympathetic
manifestations such as tachycardia, hypertension and
dilatation of the pupils may also occur. Tonic phase lasts
for a minute and is followed by “clonic phase”
characterized by jerky movements for a few minutes.
Subsequently the patient goes in a state of muscular
flaccidity and unresponsiveness (post-ictal phase). There
may be bladder or bowel incontinence. Patient gradually
regains consciousness over minutes to hours and may
Neurology 141
have post-ictal headache, confusion, muscle ache and
fatigue for hours.
Absence Seizures (Petit mal)
This occurs in childhood and ceases after 20 years of
1
age. This is characterized by brief lapses of sensorium
with loss of postural control. These are too subtle to be
noticed or referred to as day dreaming. The attacks are
much briefer (seconds) and more frequent than complex
MEDICINE AND ALLIED
partial seizures. There is no post-ictal confusion. There
may be mild motor movements like blinking of eyes,
chewing and hand clonus. This is associated with
characteristic EEG pattern.
Causes of Seizures
The etiology depends on the age of the patient. Hypoxia,
metabolic derangements, congenital defects and birth
trauma are important causes of seizures in neonates.
Febrile seizures are more common in early childhood.
Head trauma is common cause of seizures in young
adults. In older people, cerebrovascular disease, tumors
and degenerative disorders are important cause of
seizures. Metabolic and electrolyte imbalance, drugs, and
systemic illnesses can cause seizures at any age.
Investigations
1. Electroencephalogram (EEG): This may help in the
diagnosis and classification of seizure disorders.
Characteristic EEG changes in petit mal seizures (3
Hertz spike and wave activity) differentiate it from
complex partial seizures.
2. Brain imaging: CT or MRI is indicated in patients
with focal seizures, focal neurological signs or if
age of onset is more than 20 years .
3. Metabolic: Serum electrolytes, urea, calcium, blood
glucose and liver function tests are done to rule out
any metabolic cause.
4. Other tests: Blood count, ESR, X-ray chest, CSF
examination, ANA, and other specific tests may be
needed to diagnose infective or inflammatory
causes.
Differential Diagnosis
The seizures should be differentiated from transient
ischemic attacks (TIA), syncope. Pseudoseizures do not
occur during sleep and are not associated with
unconsciousness, cyanosis, incontinence and tongue bite.
 142 Textbook of Family Medicine
There are no post-ictal headache, confusion and focal
neurological deficit. EEG changes and high serum
prolactin level are features of “true” seizures and not
found in pseudoseizures. Pseudoseizures may occur in
1 hysterical reactions and malingering and may be
precipitated by emotional stress.
Management
General Precautions
MEDICINE AND ALLIED
The patient should refrain from working with dangerous
equipments and should avoid swimming, fishing, or
cycling. He should also avoid any activity such as
driving where loss of consciousness is dangerous. The
patient should avoid working near fire or at a height.
These precautions should be taken until a good control of
seizures is obtained.
Table 3: The Anti-epileptic drugs
Immediate Care of Seizures
The patient is shifted to a safer place, away from danger
(water, fire, and machine). The patient is turned to the
semi-prone position to prevent aspiration. The patient
should not be left alone until full recovery from seizures
as there may be drowsiness and confusion in the post-
ictal stage or the seizures may reoccur. Nothing should
be given by mouth until the patient has fully recovered.
If convulsions continue for a prolonged duration (> 5
minutes) or reoccur without the patient regaining
consciousness, hospitalization is a must.
Treatment of the Underlying Condition
If the cause of seizures is a metabolic abnormality
(electrolyte abnormality or glucose abnormality) it
should be corrected effectively. In case of drug induced
seizures, the offending drug should be withdrawn.
Structural CNS lesions like brain tumor, abscess, and
vascular malformation must be treated appropriately. The
antiepileptic treatment may not be required once the
underlying condition has been well treated.
Avoidance of Precipitating Factors
Seizures may be precipitated by specific trigger factors
such as sleep deprivation, alcohol withdrawal, mental
stress, physical exhaustion, flickering lights (TV or
monitor), music, loud sounds and drug abuse. Such
situations should be avoided.
Antiepileptic Drug Therapy
Drug treatment to prevent seizures is indicated in
patients with recurrent seizures of unknown etiology or
when known cause of seizures cannot be reversed.
Choice of medicine depends on the type of seizures
(Tables 3 and 4). Treatment should be initiated with a
single drug. Dose of the drug should be gradually
increased until seizures are controlled or side effects
appear. If seizures are not controlled by a single drug, a
second drug is added while the first drug is gradually
withdrawn. In most patients, seizures can be controlled
by a single drug. In some, a combination of two or more
drugs is required to control the seizures. If seizures are

refractory to medical treatment, the patient may benefit
from surgical interventions.
Monitoring
Patient should be monitored for the side effects of the
medication. Blood counts, liver function tests, renal
function tests are done at regular intervals. Serum level
of drug can be measured to guide appropriate dosage and
to check the compliance.
Duration of Therapy
Treatment should be continued until there have been no
seizures for at least 2-3 years. The dosage of the drugs
should be tapered and withdrawn gradually over 2-3
months.
Choosing AEDs
We advise initially either carbamazepine (focal seizures)
or sodium valproate (focal or generalised seizures).A
Women of childbearing potential (including girls
requiring AED into their childbearing years) should
probably not be prescribed valproate as first line
treatment because of teratogenicity. Lamotrigine seems a
safer alternative. Alternative monotherapy should be
tried before considering polytherapy. Vigabatrin is no
longer started (except in babies with West syndrome)
because of problems with permanent visual field
constriction. The role of some of the newer drugs
(gabapentin, levetiracetam, oxcarbazepine, pregabalin,
tiagabine, topiramate) will become clearer over time.
Table 4: The choice of anti-epileptic drugs
Type of epilepsy Drug(s) of choice
Partial or secondary generalized Carbamazepine
Seizures Phenytoin
Valproic acid
Primary generalized seizures Valproic acid
Lamotrigine
Absence seizures Valproic acid
Ethosuximide
Myoclonic Valproic acid
Clonazepam
Stopping AEDs
Seizure free patients require detailed discussion before
stopping AEDs. In children it is usual to try after two
years seizure free. In adults, continued seizure freedom
for driving and employment often justifies the
Neurology 143
inconvenience of continued drug treatment; many adults
therefore continue taking AEDs while seizure free for
years. Women wishing to conceive naturally want to stop
AEDs (see below), and often do so without consulting
their doctor. 1
Overall, 40% of adults seizure free for two years will
relapse. The risk is highest with previous tonic-clonic or
myoclonic seizures, seizures after starting AEDs,
needing more than one AED, and in those with abnormal
MEDICINE AND ALLIED
EEGs.The greater likelihood of seizures in the months
after withdrawal.
Follow Up
Epilepsy, more than many chronic disorders, justifies
longterm follow up. The diagnosis is history based and
too often is made incorrectly, particularly in non-
specialist hands. The choice and need for prescribed
AEDs may be inappropriate, and patients may too easily
accept drug side effects and unnecessary lifestyle
restrictions. Good practice would suggest annual review.
Proactive review of those currently managed in the
community may also be justified to check diagnoses,
optimize clinical management, and to provide
information.
Conclusion
Epilepsy clinics provide a multidisciplinary focus for the
diagnosis and long term management of patients with
recurrent blackouts and epilepsy. The diagnosis is
clinical rather than investigation based, and the emphasis
of management is long term, team delivered, and
founded upon a partnership of specialist care with the
patient and with primary care, sharing information,
supporting and empowering patients, and aiming for
their increasing independence.
STATUS EPILEPTICUS
Status epilepticus refers to continuous seizure activity or
intermittent seizures with impaired consciousness in
interictal period. This can be convulsive (tonic clonic) or
non-convulsive type. Practically seizure activity lasting
for more than 5 minutes should be managed as status
epilepticus.
Causes
Abrupt drug (anti-epileptic drugs) withdrawal or non-
compliance is the most common cause of the status
epilepticus. Other causes are metabolic disorders,
intracranial infections and structural lesions of the brain.
 144 Textbook of Family Medicine
Management
The status epilepticus should be treated as emergency.
The patient should be hospitalized.
1 1. Airway is maintained and oxygen is administered.
2. Intravenous line is started, a blood sample is
withdrawn for laboratory analysis and intravenous
dextrose (50% dextrose 25-50 ml) is promptly given.
The initial laboratory tests include glucose,
MEDICINE AND ALLIED
electrolytes, calcium, urea, creatinine, liver
transaminases and complete blood count.
3. Intravenous diazepam (10 mg) or lorazepam (4 mg)
is given slowly in two minutes. This can be repeated
once after 15 minutes if seizures are not controlled.
4. If seizures continue beyond 30 minutes, intravenous
phenytoin (20 mg/kg) at a rate not more than 50
mg/min is given. Alternatively fosphenytoin can be
given. This may be repeated in a dosage of 5-10
mg/kg. One should monitor for cardiac arrhythmia
and hypotension.
5. Phenobarbitone (IV 20 mg/kg) at a rate not more
than 50 mg/min is given if seizures are still
uncontrolled. An additional dose of 5-10 mg/kg may
be repeated if needed. Respiratory depression and
hypotension are important adverse events.
6. Uncontrolled seizures are finally managed by
general anesthesia and neuromuscular blockade
along with ventilatory support. Anesthetic agents
used are midazolam, propofol, and pentobarbitone.
7. Once the status is controlled, long-term anti-
epileptic medications are started.
8. The underlying cause is identified if any and treated
accordingly.
Complications
Important complications of status epilepticus are
cardiorespiratory dysfunction, hyperthermia, rhabdo-
mylosis, and irreversible neurological damage.
 Neurology 145

Chapter 3
STROKE
Manoj. S, S K Sharma
1

Stroke is a major public health problem. Moreover, it can

MEDICINE AND ALLIED

often be prevented, and may now be treatable in the
acute stage.
Stroke is characterized by a sudden or rapidly developing
loss of cerebral function without any other cause than
vascular, and includes both infarcts and hemorrhages.
EPIDEMIOLOGY
The incidence of stroke is now higher than that of acute
coronary syndromes. Patients with incident strokes are
the target for acute stroke management Stroke is the most
prevalent neurological disorder under the age of 85
years. Patients with prevalent stroke and transient are
chaemic attacks (TIA) are the target for secondary
prevention. Stroke is associated with increased long-term
mortality, residual physical, cognitive, and behavioural
impairments, recurrence, and increased risk of other
types of vascular event, such as myocardial infarction.
IS THIS PATIENT HAVING A STROKE
1. Sudden onset of
symptoms and signs, either all at once within
seconds or developing over few minutes, and often
worsening over the next minutes or hours, then
stabilizing and improving over time.
2. Focal symptoms and
signs, that is, generally explained by a single lesion
in the ‘Negative’’ symptoms, that is, suggesting
loss of function. Symptoms may (rarely) be
‘‘positive’’—for example, jerking of a limb,
seizure, paraesthesia, seeing flashing lights, visual
hallucinations, or movement disorders.
WHAT TYPE OF STROKE IS IT

Table 1: Causes of stroke Intracerebral hemorrhage accounts for about 20% of all,
Ischemic stroke and presents in much the same way as ischaemic stroke.
Thrombosis Although some symptoms are more frequent in ICH (for
- Lacunar infarction example, headache, impairment of consciousness at
- Large vessel thrombosis onset, epileptic seizures), none is specific enough for
Embolic
diagnosis in an individual patient. Brain imaging is
- From artery
- Carotid bifurcation mandatory to differentiate ischaemic stroke from
Cardioembolic ICH. This is crucial because ICH and ischaemic
- Atrial fibrillation stroke patients require different diagnostic work-up,
- Myocardial infarction acute treatment and secondary prevention., a brain
- Infective endocarditis CT-scan without contrast should be performed, mainly to
- Valvular lesions differentiate ICH (hyperdensity in the brain parenchyma)
Others
from ischaemic stroke, and to diagnose structural mimics
- Hypercoagulable states
- Vasculitis of stroke (subduralhaematoma, tumor etc).
- Meningitis
Hemorrhagic TRANSIENT ISCHAEMIC ATTACKS
- Hypertension
- Trauma The classical definition is an acute loss of focal cerebral
- Anticoagulant therapy or monocular function with symptoms lasting less than
- Aneurysm 24 hours, with no other explanation than an inadequate
- AV malformation blood supply’. The major difficulty with TIA patients
- Blood dyscrasias (and sometimes physicians) is that, often, they do not
- Brain tumor
consider the symptoms as an emergency, because they
 146 Textbook of Family Medicine
resolve. This is important because some of these patients
have a high risk of ischaemic stroke, and half the patients
who do have a stroke after a TIA do so within a week
and some are preventable. Like strokes, TIAs are an
1 emergency, at least when seen within the first few days.
DIFFERENTIAL DIAGNOSIS OF STROKE
1 Migraine aura:
2. Focal epilepsy:
3. Transient global amnesia
MEDICINE AND ALLIED
4. Structural brain lesions, chronic subdural
haematoma, meningioma, intracranial venous
thrombosis, etc
5. Hypoglycaemia
6. Multiple sclerosis
7. Labyrinthine disorder
8. Mononeuropathies
IN ALL PATIENTS THE FOLLOWING ARE
NECESSARY
Clinical examination, especially for cardiac
abnormalities and arterial pulses/bruits.
Full blood count to detect polycythaemia and
thrombocythaemia.
Raised erythrocyte sedimentation (ESR) orC-reactive
protein to detect vasculitis, infections, etc.
Blood glucose to detect diabetes, or hypoglycaemia in
the acute situation.
Urea and electrolytes (baseline) and blood cholesterol
(risk factor).
ECG to detect atrial fibrillation and acute myocardial
infarction.
Cervical artery ultrasonography to detect stenosis or
occlusion, or dissection.
Optional investigations are guided by the results of the
initial investigations, age, and the clinical context:
Angiography (MR, CT or catheter). Transthoracic
echocardiography to detect intracardiac thrombus or
tumours, valvulopathies, valvular vegetations, decreased
ventricular ejection fraction, patent foramen ovale (trans
oesophageal echocardiography if necessary).
24-hour ECG if intermittent arrhythmia suspected.
Specialised biological tests when a specific cause is
suspected, such as antinuclear and anticardiolipin
antibodies, syphilis serology
WHAT IS CAUSING THIS STROKE OR TIA?
Ischaemic strokes and TIA the most frequent causes are
large-artery atherosclerosis (about 50%), atrial
fibrillation (about 25%), and small vessel disease of the
deep perforators (about 20%), and in young patients the
leading cause is arterial dissection . In other populations
the causes are somewhat different, particularly
valvulopathies and infectious disorders
INTRACEREBRAL HAEMORRHAGE
Most cases not due to an intracranial vascular
malformation are due to small-vessel disease (a
consequence of chronic arterial hypertension) or cerebral
amyloid angiopathy (generally lobar hemorrhage).
Treatment
Following are main components of management of
stroke;
1. Medical support: The patient should be urgently
hospitalized. The medical management includes
control of blood pressure, maintenance of fluid and
electrolytes, and control of intracranial pressure
(with IV mannitol).
2. Thrombolysis: This is indicated in early ischemic
stroke within 4.5 hours of onset of symptoms.
Recombinant tissue plasminogen activator (rTPA) is
used for thrombolysis.
Contraindications to thrombolysis (stroke)
 Haemorrhage on CT scan
 Arteriovenous malformation / Aneurysm
 Seizures
 Hypertension (BP >220/130)
 Surgery / recent trauma
 Liver disease, varices or portal hypertension
 Anticoagulant therapy (patient already on) or
PPT (prothrombin time) >15s
 Platelets <100×10^9/L
3. Aspirin in the doses of 160-325 mg daily is indicated
for acute and long-term management of ischemic
stroke.
4. Anticoagulation is required to prevent recurrent
embolic strokes. Warfarin is used for chronic
anticoagulation and the target INR should be 2-3 (in
case of prosthetic valve 2.5-3.5).
5. Carotid endarterectomy is indicated in patients with
>70 percent carotid stenosis. It decreases the risk of
stroke and death.
6. Modification of risk factors includes the control of
blood pressure, blood sugar, serum lipids, and
cessation of smoking.
7. Physiotherapy and rehabilitation

Non-specific management
Detection and management of life-threatening
emergencies (aspiration, status epilepticus, respiratory
arrest, etc).
Stabilization of physiological parameters (hypoxaemia,
hyperglycaemia, hyperthermia,decreased cardiac output,
and deyhydration),especially during the first days, with
the exception of blood pressure because there is transient
loss of auto regulation of cerebral blood flow. Therefore,
although there are no evidence-based data, high blood
pressure should not be treated in the acute stage unless
there is an associated life-threatening disorder such as
aortic dissection or ICH
Early prevention of complications:– Pressure sores:
appropriate caloric intake, early mobilization and
appropriate beds and nursing.
Aspiration pneumonia: detection of swallowing
impairment and nasogastric tube when necessary.
• Deep venous thrombosis and pulmonary embolism:
low molecular weight heparin reduces the risk but
has no overall effect on mortality (because it
increases the risk of intracranial and extra cranial
bleeding).
• Rehabilitation can be started as soon as the patient is
stable: passive measures minimize the risks of
contractures, pressure sores and pneumonia.
• Stroke unit care provides coordinated
multidisciplinary input, with continuous training of
specialized staff members, and reduces mortality and
dependency, in part by the prevention of non-
specific complications that occur in the first days.
Specific management of ischaemic stroke
Antithrombotic therapy- Aspirin 300 mg at once and then
75–150 mg daily prevents 15 dependencies or deaths
per1000 patients treated.
Thrombolytic therapy Intravenous recombinant tissue
plasminogen activator (rt-PA) increases the odds of a
favourable outcome at 3 months by about eight times if
given within 90 minutes of onset, and by about twice
within 91–180 minutes. Case fatality is not affected if
given up to270 minutes, but increases thereafter.
Hemorrhagic transformation is associated with
increasing age, and large infarcts. The main messages are
the sooner rt-PA is given, the greater the benefit, and
Neurology 147
there may be potential benefit beyond 3 hours, but with
some risks. The dose is 0.9 mg/kg (10% as an iv bolus,
then 90% as a continuous iv injection over1 hour).
Surgery- In large cerebellar infarcts with hydrocephalus
or brainstem compression, ventricular drainage or 1
posterior fossa decompression are recommended
Decompressive hemicraniectomy reduces mortality and
disability in patients with large infarcts in the middle
cerebral artery territory. Decompressive
hemicraniectomy is beneficial only if conducted within
MEDICINE AND ALLIED
48 hours of ictus.
Specific management of Intracerebral hemorrhage
Blood pressure management-Reducing blood pressure in
acute ICH may prevent hematoma growth and decrease
the risk of re bleeding, but also reduces perfusion
pressure and may compromise cerebral blood flow.
Based on these considerations, an upper limit of systolic
blood pressure of180 mm Hg and a diastolic blood
pressure of105 mm Hg is recommended before treatment
is necessary; the target blood pressure should be 170/100
(or a mean blood pressure of125 mm Hg). For patients
without known hypertension ,the upper recommended
limits are 160/95 mm Hg before treatment is necessary;
the target should be 150/90 (or a mean of 110 mm Hg).
Intravenous labetalol, enalapril, sodium nitroprusside are
used.
Prevention of deep venous thrombosis- Graded
compression stockings are effective in surgical patients,
but their efficacy in stroke patients when they can only
be fitted after the initiating event is still being tested.
Although subcutaneous unfractionated and low
molecular weight heparins reduce venous
thromboembolism, their effect is counterbalanced by an
increase in hemorrhagic complications.
Increased intracranial pressure-The main methods of
medical decompression include hyperventilation,
osmotic diuretics, and intravenous barbiturates.
Corticosteroids should be avoided.
RISK FACTORS FOR STROKE
Non-modifiable risk factors - increasing age, male
gender, and familial predisposition)
Modifiable risk factors –
a) Blood pressure. The risk of stroke doubles for every
7.5 mm Hg increase in diastolic blood pressure
b) Blood cholesterol: there is a somewhat increased risk
of ischaemic stroke with increasing total and LDL
cholesterol levels, and decreasing HDL cholesterol.
Many patients with ICH have normal or even low
cholesterol levels.
c) Cigarette smoking doubles the risk of ischaemic
stroke.
 148 Textbook of Family Medicine

d) Diabetes mellitus doubles the risk of ischemic stroke,

independently of other factors.
e) Oral contraceptives.
THE OUTCOME AFTER STROKE
1 Any type of stroke (ischaemic and hemorrhagic)
Long-Term Outcome

Dementia is a major cause of dependency after stroke; in

Short-Term Outcome
Early epileptic seizures (2weeks after stroke onset) occur
in about 5% of patients, more likely with a cortical lesion
MEDICINE AND ALLIED
about 30%. Post-stroke dementia may be due to any
combination of vascular lesions, Alzheimer pathology
and leukoaraiosis. Post-stroke depression occurs in up to
half of stroke survivors and remains high over time. Late

and a more severe stroke. Delirium occurs in one quarter
of stroke patients, more frequent in those with pre-
existing cognitive decline and who develop metabolic or
infectious complications. Large cerebellar strokes may
lead to hydrocephalus or direct compression of the
brainstem, usually between 48 and 96 hours in infarcts,
earlier in haemorrhages. Non-specific complications
include pressure sores, pneumonia, urinary tract
infection, hyponatraemia, deep venous thrombosis and
pulmonary embolism. They are all more frequent in
patients with severe neurological deficits.
epileptic seizures (.2weeks after stroke onset) occur in
about 4% of patients, particularly with cortical lesions,
severe strokes, and associated dementia. Physical
sequelae (motor or sensory deficits, pain, hemianopia)
and neuropsychological deficits (aphasia, neglect,
emotionalism, anxiety)are other major components of
post-stroke disability.

Chapter 4
COMA
Manoj S,
Definition
Altered mental state or encephalopathy may range from
mild confusion to total unresponsiveness. At one end of
the spectrum, stupor and coma refer to a state of near or
total unresponsiveness and can be caused by either a
focal or diffuse process. In this review, we discuss the
general approach to patients with stupor and coma.
Timely diagnosis and appropriate treatment are important
because stupor and coma often reflect life-threatening,
systemic or intracranial processes.
ANATOMY OF COMA
Consciousness is contingent on the integrity of bilateral
cerebral hemispheres and the reticular activating system
in the brain stem. Focal lesions such as stroke or
hemorrhage of the brain stem cause coma by disrupting
the reticular activating system. Coma also results from
derangement of bilateral cerebral hemispheres, such as
that caused by infection, drug or alcohol intoxication, or
a systemic disease like hepatic encephalopathy and
hyperosmolarity. A unilateral focal lesion affecting only
one cerebral hemisphere, such as middle cerebral artery
stroke, seldom causes coma. In these cases, coma results
only when the contralateral hemisphere is also impaired,
either from a preexisting disease (eg, previous stroke) or
secondarily from swelling or herniation originating in the
affected hemisphere (eg, large tumor or hemorrhage).
CAUSES OF COMA
Comas are caused by an injury to the brain. Brain injury
can be due to increased pressure, bleeding, loss of
oxygen, or buildup of toxins. The injury can be
temporary and reversible. It also can be permanent.
More than 50% of comas are related to head trauma or
disturbances in the brain's circulatory system.
Problems that can lead to coma include:
 Trauma: Head injuries can cause the brain to swell
and/or bleed. When the brain swells as a result of
trauma, the fluid pushes up against the skull. The
swelling may eventually cause the brain to push
down on the brain stem, which can damage the RAS
(Reticular Activating System) -- a part of the brain
that's responsible for arousal and awareness.
Neurology 149
1
Neeta Bhargava
 Swelling: Swelling of brain tissue can occur even
MEDICINE AND ALLIED
without distress. Sometimes a lack of oxygen,
electrolyte imbalance, or hormones can cause
swelling.
 Bleeding: Bleeding in the layers of the brain may
cause coma due to swelling and compression on the
injured side of the brain. This compression causes the
brain to shift, causing damage to the brainstem and
the RAS (mentioned above). High blood pressure,
cerebral aneurysms, and tumors are non-traumatic
causes of bleeding in the brain.
 Stroke: When there is no blood flow to a major part
of the brain stem or loss of blood accompanied with
swelling, coma can occur.
 Blood sugar: In people with diabetes, coma can
occur when blood sugar levels stay very high. That's
a condition known as hyperglycemia. Hypoglycemia,
or blood sugar that's too low, can also lead to a coma.
This type of coma is usually reversible once the
blood sugar is corrected.
 Oxygen deprivation: Oxygen is essential for brain
function. Cardiac arrest causes a sudden cutoff of
blood flow and oxygen to the brain, called hypoxia or
anoxia. After cardiopulmonary resuscitation (CPR),
survivors of cardiac arrest are often in comas.
Oxygen deprivation can also occur with drowning or
choking.
 Infection: Infections of the central nervous system,
such as meningitis or encephalitis, can also cause
coma.
 Toxins: Substances that are normally found in the
body can accumulate to toxic levels if the body fails
to dispose of them correctly. As an example,
ammonia due to liver disease, carbon dioxide from a
severe asthma attack, or urea from kidney failure can
accumulate to toxic levels in the body. Drugs and
alcohol in large quantities can also disrupt neuron
functioning in the brain.
 Seizures: A single seizure rarely produces coma. But
continuous seizures -- called status epilepticus -- can.
Repeated seizures can prevent the brain from
recovering in between seizures. This will cause
prolonged unconsciousness and coma.
 150 Textbook of Family Medicine

PATIENT EXAMINATION IN A CASE OF COMA
1 Airway, Breathing, Cardiac status: check gag reflex
and ability to protect airway
1 2 Assess level of consciousness to verbal, physical,
and painful stimuli
3 Assess nuchal rigidity
4 Initiate empiric treatment if appropriate
5 Document pupil size and reflex to a bright light
6 Note whether any spontaneous eye movements
occur; if not, perform doll’s eyes maneuver or cold
MEDICINE AND ALLIED
upper brain stem adjacent to the brain-stem reticular
activating system. Intactness of these pathways in a
comatose patient generally excludes a brain stem lesion
and points instead to bilateral cerebral hemispheric
dysfunction. Bilateral hemi hemispheric dysfunction, in
turn, usually suggests a diffuse intracranial process or a
systemic derangement. The size and reactivity of the
pupils offer an important clue to the origin of coma.
Symmetric, reactive, but unusually small or large pupils
are commonly caused by drug ingestions. One caveat is a
pontine lesion (most commonly due to a stroke or

water caloric test hemorrhage), which causes small but reactive pupils and
7 Rate motor function: spontaneous purposeful impaired eye movements. The pupillary reflex also
movement, withdrawal to pain, or abnormal provides an early clue to an impending transtentorial
posturing to pain herniation. Uncal herniation from an expanding lesion in
8 Look for asymmetry of limb movements, stretch one of the cerebral hemispheres (for example, subdural
reflexes, and Babinski sign hematoma or swelling from a large stroke) typically
9 Do fundoscopic examination to look for stretches the third nerve, leading to asymmetric pupillary
papilloedema and retinal hemorrhage dilatation on the side of the lesion. Other signs of third
10 Physicians should also be familiar with the Glasgow nerve palsy, such as ipsilateral ptosis and abnormal eye
Coma Scale movements, may also be seen. Physician should also
note whether both eyes move in a coordinated way—
Table 1: Glasgow Coma Scale conjugate eye movements. Spontaneous and conjugate
Eye opening roving eye movements with nearly normal range imply
intact brain stem function and often accompany
Never - 1
metabolic encephalopathy. Gaze preference to one side
To pain - 2 suggests either a brain stem lesion or an asymmetric
To verbal stimuli - 3 impairment of the cerebral hemispheres. When eye
Spontaneous - 4 movements are absent or incomplete, they should be
Best verbal response assessed further by passively turning the patient’s head
No response - 1 from side to side (the oculo cephalic or “doll’s eyes”
maneuver). If the oculo cephalic reflex is absent, a
Incomprehensible sounds - 2
stronger stimulus from the ice water caloric test may be
Inappropriate words - 3 used. After checking that the tympanic membrane is
Disoriented and converses - 4 intact, irrigate the external auditory canal with 10 ml of
Oriented and converses - 5 ice water using a syringe connected to a flexible catheter.
Best motor response If performed on a healthy conscious person, the stimulus
None - 1 will reliably evoke vertigo and nystagmus, with fast
phase of the nystagmus directed away from the irrigated
Extensor posturing - 2
ear. In a comatose patient with intact brain stem function,
Flexor posturing - 3 a tonic deviation of both eyes toward the stimulated ear
Withdrawal - 4 occurs instead.
Localized pain - 5
Obeys - 6 In patients with stupor or coma, sensory and motor
functions are assessed by applying painful stimuli to the
supra orbital ridge, the nail bed of each limb, or the
sternum. The physician should look for facial grimacing,
Which is useful for the assessment of prognosis and
purposeful withdrawal of each limb from the painful
longitudinal monitoring of neurologic status? The
stimulus, or decorticate or decerebrate posturing of the
neurologic examination has two goals: to test whether
upper and lower limbs. Decorticate posturing involves
the brain stem is intact and to detect any asymmetry that
flexion and adduction of the arms and extension of the
may suggest a focal process. Begin the examination by
legs. Decerebrate posturing consists of internal rotation
observing the patient’s spontaneous activity and response
of the extended arms and extension of the legs. Both
to verbal and physical stimuli.
indicate a gross and often life-threatening dysfunction in
The pupillary reflex and eye movement pathways are the brainstem or cerebral hemispheres. Close observation
especially important because they are located in the and comparison between sides are important.
Asymmetric motor response to pain, manifesting as

either asymmetric posturing or lack of movement on one
side of the body, often provides the only clinical clue to a
focal hemispheric lesion.
In a patient with some spontaneous movements, the
inability to hold up one arm against gravity or
preferential movement of limbs on one side are also
important signs of an asymmetric process. The
examination is then followed by evaluation of the tendon
stretch reflexes and the plantar response, looking for a
Babinski sign. Asymmetric reflexes or Babinski sign
may corroborate the impression of a hemiparesis noted in
the testing of response to pain. Subtle differences in a
comatose patient are generally too nonspecific to be of
localizing value.
The examination should also include a fundoscopic
examination to look for papilledema and neck flexion to
assess possible meningeal irritation (if there is no reason
to suspect cervical spine instability). Nuchal rigidity in a
patient in coma may indicate an infectious process,
subarachnoid hemorrhage, or impending herniation.
FURTHER EVALUATION
After the initial examination is done and the patient is
stabilized, further history regarding events leading to the
coma, past medical conditions, drug and medication use,
and social history are often helpful in reaching an
eventual diagnosis. Routine studies such as a complete
blood cell count, complete metabolic panel, arterial
blood gas measurements, electrocardiography, and chest
radiography should be done on all patients with altered
mental state. Patients with a possible metabolic cause of
encephalopathy should have a toxicology screen as well.
Unless a metabolic cause of coma is immediately evident
(for example, drug overdose and hyper osmolar coma),
an imaging study of the brain is unavoidable. In most
centers, computed tomography is more readily available
than magnetic resonance imaging, although the latter
provides superior anatomic information. The possibility
of infection should prompt blood and urine cultures and a
lumbar puncture, once the imaging study clears any risk
of herniation. Any lumbar puncture should include
measurement of the opening pressure with the patient in
a supine position and cerebrospinal fluid analysis of cell
and differential counts, protein, glucose, Gram’s stain,
and other microbiologic studies.
Neurology 151
Most patients with stupor and coma require intensive
care monitoring. The most common criteria for
admission to the intensive care unit (ICU) are
requirement for cardiac or ventilator support and a
precariously unstable neurologic state.
1
TREATMENT
It is usually guided by the underlying cause of coma.
Intravenous thiamine, dextrose, and naloxone are
relatively safe and may be given empirically.
MEDICINE AND ALLIED
PROGNOSIS
The probability of recovery depends on the initial cause
and the severity of the coma. Coma of metabolic causes
is in general reversible, unless the clinical course is
complicated by secondary anoxic injury to the brain. It is
more difficult to determine prognosis in patients with
coma due to structural lesions. The nature and
reversibility of the lesion and the timing of intervention
are important determinants. Some general guidelines are
available from studies of patients with no penetrating
traumatic coma. A Glasgow coma score of 9 or higher is
associated with a favorable prognosis, whereas a loss of
pupillary reflex, doll’s eye sign, or a Glasgow coma
score of less than 5 are associated with poor recovery.
In caring for patients with stupor and coma, all
physicians should be familiar with the key steps of the
neurologic examination. Proper observation helps with
the initial localization and diagnosis and with the
subsequent determination of the prognosis. This, together
with supportive data such as medical history, laboratory
test results, and brain imaging, will further guide timely
and appropriate treatment.
 152 Textbook of Family Medicine

Chapter 5
SYNCOPE
1 A K Tripathi, Kamal K Sawlani

Syncope is defined as a transient loss of consciousness  The vasovagal syncope occurs generally in the
due to diminished cerebral perfusion. Syncope is
MEDICINE AND ALLIED

sitting and standing posture. Hence, it is

characterized by loss of postural control and spontaneous essential that the patient is immediately made to
recovery. lie down (recumbent position) at the earliest.
It may be preceded by symptoms of ‘presyncope’ such as  Venous pooling which may occur during
lightheadedness, visual blurring, dizziness, sweating and prolonged standing or sitting posture reduces
nausea. the filling of the ventricle. The underfilled
ventricle vigorously contracts due to increased
Causes of Syncope sympathetic activation which in turn stimulate
The causes of syncope can be classified into: myocardial mechanoreceptors and vagal
(1) cardiovascular disorders afferent fibers. This causes vasodilation (due to
(2) vascular disorders sympathetic inhibition) and bradycardia
(3) cerebrovascular diseases (increased parasympathetic activity).
Vasodilatation and bradycardia produce
Table 1: Causes of syncope hypotension and syncope.

1. Disorders of vascular tone and blood volume Postural Hypotension (Postural Syncope)
Vasovagal syncope  Postural hypotension (orthostatic hypotension,
Postural hypotension OH) is a fall in systemic arterial pressure on
Carotid sinus sensitivity assumption of upright posture. It is defined as a
Cough or micturition syncope sustained drop in systolic (>20 mm Hg) or
diastolic (> 10 mm Hg) blood pressure within 3
2. Cardiovascular disorders minutes of standing.
Arrhythmias  The common causes of postural (orthostatic)
Sinus bradycardia hypotension are defective postural reflexes and
Heart blocks drugs. There is fall in the systemic arterial
Ventricular and supraventricular pressure on assumption of an upright posture.
tachycardia  These defective postural reflexes are generally
Aortic stenosis due to autonomic peripheral neuropathy such as
Hypertrophic obstructive cardiomyopathy in diabetes, parkinsonism and aging.
Left ventricular dysfunction  Hypovolemia because of diuretic therapy,
3. Cerebrovascular disease excessive sweating, diarrhea, or hemorrhage
Vertebrobasilar insufficiency may also lead to postural syncope.
Basilar artery migraine  Drugs that cause postural syncope mainly
Conditions which resemble syncope include vasodilators, diuretics and
Hysterical fainting antidepressants.
Anxiety
Hypoglycemia Cardiac Syncope
Seizures
Arrhythmia is the most common cause of syncope due to
Vasovagal Syncope cardiac cause. The syncope can occur in profound
 This is the most common cause of “common bradycardia or tachyarrhythmia. Under these conditions,
faint” in normal persons. the decreased stroke volume can lead to cerebral
hypoperfusion. The syncope due to atrio-ventricular
 The precipitating factors are hot or crowded
block is known as Stokes-Adams attack.
environment, severe pain, extreme fatigue,
prolonged standing, hunger, and emotional
situations.
 Neurology 153

Seizures and Syncope Immediate Actions to be Taken During Syncope

• The patient should be placed in supine position with
The seizures may easily be confused with syncope.
head tilted to the side to maximize cerebral blood
However, careful history and examination may reliably
flow and to avoid aspiration.
differentiate these situations. The important differences
are listed in Table 2.
• Clothing should be loosened.
1
Table 2: Differences between syncope and seizures
Seizure Syncope

Premonitory symptoms None or aura Lightheadedness, nausea, blurring of vision

MEDICINE AND ALLIED

Rapidity of onset Immediate Gradual

Period of unconsciousness Prolonged (minutes) Transient (seconds)

Facial appearance Cyanosis and frothing
Precipitating factors Usually none
Posture Any posture
Associated findings Motor seizures, tongue biting,
urinary incontinence
Recovery Prolonged headache, confusion,
focal neurological signs
Pallor, Sweating, palpitation
Emotional stress, postural
hypotension, prolonged standing
Usually erect
Motor movement uncommon and transient
Rapid and uneventful

Investigations • The patient should not be allowed to rise again till

Tests like ECG, echocardiography, Holter ECG and
electrophysiological studies may be needed to diagnose
the cause of syncope. Upright tilt test is used to confirm
the diagnosis of vasovagal syncope. Other tests like
EEG, CT, MRI scan may be needed to diagnose any
neurological cause.
Treatment
The treatment depends upon the underlying cause.
However, certain precautions are to be taken regardless
of the cause.
weakness persists.
• Peripheral stimulation like sprinkling cold water over
the face may help.
Instructions to the Patients
• Patients should try to assume a recumbent position as
soon as they feel premonitory symptoms.
• Patients are advised to avoid situations that have
caused the syncope.
• Patients who have recurrent syncope should avoid
climbing ladders, swimming alone, driving or
operating machines.
 154 Textbook of Family Medicine
Chapter 6
FACIAL NERVE PASLY
1 A K Tripathi,
The facial nerve (VII cranial nerve) arises from the pons,
MEDICINE AND ALLIED
passes through the facial canal and exits from the skull
though stylomastoid foramina. It then passes through the
parotid gland and subsequently divides into branches It
provides motor innervation to all muscles of the facial
expression and the stapedius. Through its branch, the
chorda tympani, it carries taste sensation from the
anterior two-thirds of the tongue. It also carries
cutaneous impulses from the anterior wall of the external
auditory canal.
Causes of the Facial Nerve Palsy (Infranuclear)
The involvement of facial nerve at its origin in the
pons or at any site throughout its course may lead
to infranuclear facial palsy (lower motor neuron
type).
Table 1: Causes of infranuclear facial nerve palsy
Pons: Infarction, tumor, multiple
sclerosis
Cerebellopontine Acoustic neuroma
angle:
Temporal bone: Chronic suppuratve otitis media
(CSOM), cholesteatoma, Bell’s
palsy, Ramsay Hunt syndrome,
dermoid, carotid body tumor
Outside skull: Parotid lesions, trauma, lymph
node swelling
Features of Facial Nerve Palsy
There is drooping of the corner of the mouth and loss of
naso-labial fold on the affected side. There is loss of
facial expression at the side of the palsy. Furrows of the
forehead are absent. The eye is more widely open and the
eyelids do not close completely on the side of lesion..
When the patient is asked to smile or show his teeth, the
angle of the mouth at the side of the lesion does not
move.
Kamal K Sawlani
On attempted closure of the eye lids, the eye ball on the
paralyzed side rolls up (Bell’s phenomenon). Food
collects between teeth and the lips. Saliva dribbles from
the angle of the mouth on the paralyzed side. The patient
is unable to whistle or blow. There is loss of taste in the
anterior two thirds of the tongue on the same side. If the
nerve to stapedius is damaged, there is hyperacusis
(sensitivity to loud sounds). There is no sensory loss over
the face.
Localization of the Site of Lesion in
Supranuclear Facial Palsy
The damage of corticonuclear fibers from motor cortex
to facial nucleus may cause supranuclear facial palsy
(upper motor neuron type). The infranuclear facial
paralysis must be differentiated from supranuclear type
of facial palsy. In supranuclear facial palsy, the upper
part of the face (frontalis, orbicularis oculi) is involved to
a lesser extent than the lower part of the face whereas
whole of the face is equally involved in infranuclear
facial palsy. This is because upper part of the face is
innervated by both motor cortices whereas the lower part
of the face is innervated by the opposite hemisphere
only. Supranuclear facial palsy is often associated with
paralysis of the arm and leg of the same side or aphasia.
The taste sensation in the anterior two-thirds of the
tongue is not involved in supranuclear type. Emotional
facial movements are also preserved in supranuclear
type. In supranuclear type, the lesion is on the opposite
side of the palsy whereas it is on the same side of the
palsy in infranuclear type. Important causes of
supranuclear palsy are cerebral thrombosis, cerebral
embolism, cerebral hemorrhage, and brain tumor.
Infranuclear Facial Palsy
If the lesion of the facial nerve is outside the
stylomastoid foramen, only motor manifestations are
present. Taste is not involved as chorda tympani joins the
facial nerve in the facial canal before the facial nerve
emerges from the stylomastoid foramen. There is no
hyperacusis.
 Neurology 155

The lesion of the facial nerve in facial canal near the

middle ear may cause hyperacusis in addition to loss of
taste. Other cranial nerves (auditory and vestibular) are
also involved if the lesion is near the internal auditory
meatus. In the pontine lesion, sixth cranial nerve may
Investigations
1
also be involved and there may be hemiplagia of the MRI may show swelling and enhancement of geniculate
opposite side (crossed hemiplagia). ganglion and facial nerve. EMG has prognostic value.
If the recovery of motor function is incomplete, aberrant
Treatment
regeneration can cause synkinesis, i.e. movement of one

MEDICINE AND ALLIED

muscle can cause movement of another or all muscles for Symptomatic
example closure of eye can cause deviation of the angle This includes massage of the facial muscles and
of the mouth. Lacrimal gland fibres may join with fibres protection of the eye during sleep to prevent corneal
of other muscles so that while eating, tears may also flow damage. A lubricating eye drop is used to avoid dryness.
(crocodile tears). Orbicularis oculi fibers may join with
orbicularis oris resulting in the closure of eyelids when Specific
the mouth is opened (jaw winking). Administration of glucocorticoids with or without
acyclovir improves the outcome. The dose of predni-
BELL’S PALSY
solone is 60-80 mg daily for 5 days and then tapered over
This is the most common cause of facial palsy. It is a the next 5 days. Acyclovir is given in a dosage of 500 mg
type of idiopathic infranuclear (lower motor neuron type) 5 times daily for 5 days. Combination of prednisolone
facial palsy, the cause of which is not known. Bell’s with acyclovir is more effective than prednisolone alone.
palsy has been associated with reactivation of herpes
Prognosis
simplex type I infection, but its causal role is not
established. Over 80 percent of the patients recover completely in a
few weeks time. Patients with complete paralysis have a
Clinical Features
less favorable prognosis than those with incomplete
Onset is abrupt and the maximum weakness occurs in 48 paralysis.
hours. Pain about the ear may occur prior to or along
with the weakness. Motor manifestations are the same as
described above. Bell’s phenomenon is present. There is
loss of taste in the anterior two-thirds of the tongue on
the same side. There may be hyperacusis on the side of
lesion if nerve to stapedius is also involved.
 156 Textbook of Family Medicine

1
MEDICINE AND ALLIED