STROKE AND CEREBROVASCULAR DISEASE

Stroke is the second most common cause of death and a major cause of disability world-wide. The death rate following stroke is 20-25%. The inci-dence rises steeply with age; it is uncommon in those under 40 years. It is slightly more common in men. Hypertension is the most treatable stroke risk factor. A Face, Arm, Speech, Time (FAST, speech and/or arm weakness, dysphasia) is used outside of hospital by paramedics or relatives to facilitate early recognition of the symptoms of stroke and allow early action to be taken.

Definitions

Stroke is defined as rapid onset of neurological deficit (usually focal) which is the result of a vascular lesion and associated with infarction of central nervous tissue. A completed stroke is when the neurological deficit has reached its maximum (usually within 6 hours).

Stroke in evolution is when the symptoms and signs are getting worse (usually within 24 hours of onset).

A minor stroke is one in which the patient recovers without a significant neurological deficit, usually within 1 week.

Transient ischaemic attack (TIA) is a transient episode of neurologic dysfunction caused by focal brain, spinal cord or retinal ischaemia without acute infarction. TIAs have a tendency to recur and may herald thrombo-embolic stroke.

Pathophysiology

Different pathological events cause similar clinical events in cerebrovascular disease.

Completed stroke Most strokes (85%) are caused by cerebral infarction due to arterial embolism or thrombosis. Thrombosis occurs at the site of an atheromatous plaque in carotid, vertebral or cerebral arteries. Emboli arise from atheromatous plaques in the carotid/vertebrobasilar arteries, or from cardiac mural thrombi (e.g. following myocardial infarction), or from the left atrium in atrial fibrillation. In about 15% of cases stroke is caused by intra-cranial or subarachnoid haemorrhage.

Less commonly the clinical picture of stroke may be caused by intracranial venous thrombosis, multiple sclerosis relapse and a space-occupying lesion in the brain, e.g. a tumour or abscess. In the latter the onset of symptoms and signs is usually much slower than in a stroke. In young adults one-fifth of strokes are caused by carotid or vertebral artery dissection allowing blood to track within the wall of the artery and occlude the lumen. It should be considered in those with recent neck pain, trauma, or manipulation of the neck. Diagnosis is by MR angiography.

Transient ischaemic attacks TIAs are usually the result of passage of microemboli (which subsequently lyse) arising from atheromatous plaques or from cardiac mural thrombi (see stroke above). The risk factors and causes of TIAs are the same as those for thromboembolic stroke. A TIA may also be caused by a temporary drop in cerebral perfusion (e.g. cardiac dysrhythmia, severe hyper- or hypoperfusion) and rarely tumours and subdural haema-tomas may produce a similar clinical picture.

Risk factors

The major risk factors for thromboembolic stroke are those for atheroma, i.e. hypertension, diabetes mellitus, cigarette smoking and hyperlipidaemia. Others are obesity, oestrogen-containing oral contraceptives, excessive alcohol consumption and polycythaemia (hyperviscosity syndromes). Atrial fibrillation is a major risk factor for embolic stroke (rate 1-5% per year depending on age). Rarer causes of stroke are migraine, vasculitis, cocaine (by causing vasoconstriction), antiphospholipid syndrome (p. 302) amd the thrombophilias (predispose to cerebral venous thrombosis).

Transient ischaemic attacks (TIAs)

There is a sudden onset of focal neurological deficit with symptoms maximal at the onset and usually lasting 5-15 minutes; gradual progression of symp-toms suggests a different pathology such as demyelination, tumour or migraine. Symptoms and signs depend on the site of the brain involved (Table 17.8). Amaurosis fugax is painless transient monocular blindness as a result

Table 17.8 Features of transient ischaemic attacks in different arterial territories

Carotid territory symptoms

Vertebrobasilar territory symptoms

Amaurosis fugax

Diplopia, vertigo, vomiting

Aphasia

Choking and dysarthria

Hemiparesis

Ataxia

Hemisensory loss

Hemisensory loss

Hemianopic visual loss

Hemianopic or bilateral visual loss

  Tetraparesis
  Loss of consciousness (rare)

of the passage of emboli through the retinal arteries. Dizziness, loss of consciousness and temporary memory loss (transient global amnesia) occur-ring on their own are not due to TIAs. The history and physical examination must include a search for risk factors and possible sources of emboli (atrial fibrillation, valve lesion, carotid bruits in the neck).

Investigations

The diagnosis of TIA is clinical.

Blood is taken for measurement of glucose, full blood count (to identify polycythaemia), ESR (raised in the few cases of vasculitis), creatinine and electrolytes, cholesterol and INR (if taking warfarin).

Brain imaging by diffusion weighted magnetic resonance imaging (MRI) together with specialist review should be performed within 24 hours in patients with an ABCD2 score >4 (Table 17.9) or if they have crescendo TIAs (defined as two or more in a week); these patients are at highest risk of stroke. Computed tomography is used where MRI is contraindicated or unavailable. Brain imaging should be performed within 1 week in lower risk patients.

Carotid artery imaging Carotid doppler and duplex ultrasound scanning are performed (ideally within 1 week of onset of symptoms) to look for carotid atheroma and stenosis. MR angiography or CT angiography are performed if ultrasound suggests carotid stenosis to determine the degree of carotid artery stenosis.

Treatment

Antithrombotic treatment Aspirin 300 mg should be given immediately and continued long term (75 mg once daily) with modified release dipyridamole

(200 mg twice daily). Clopidogrel (75 mg daily) is given for those patients intolerant of aspirin. Long-term anticoagulation with warfarin (after brain imaging) is given to patients in atrial fibrillation, with some valvular lesions (uninfected) or dilated cardiomyopathy.

Other secondary prevention This involves advice and treatment to reverse risk factors (p. 744). Control of hypertension (p. 483) is the single most important factor in the prevention of stroke. Treatment with a statin (e.g. simvastatin 40 mg daily) should be given to patients with a total cho-lesterol >3.5 mmol/l or low-density lipoprotein cholesterol >2.5 mmol/l.

Carotid endarterectomy is recommended in patients with internal carotid artery stenosis >70%. Successful surgery reduces the risk of further TIA/stroke by about 75%. Endarterectomy had a mortality of around 3% and a similar risk of stroke.

Patients should not drive for a month after TIA.

Cerebral intarction

Most thrombolembolic cerebral infarctions cause an obvious stroke. Follow-ing vessel occlusion brain ischaemia occurs, followed by infarction. The infarcted area is surrounded by a swollen area which can regain function with neurological recovery.

Clinical features

The neurological deficit produced by the occlusion of a vessel may be pre-dicted by a knowledge of neuroanatomy and vascular supply (Figs 17.1 and 17.9). In practice it is less clear-cut because of collateral supply to brain areas.

Cerebral hemisphere infarcts The most common stroke is the hemi-plegia caused by infarction of the internal capsule (the narrow zone of motor and sensory fibres that converges on the brainstem from the cerebral cortex; Fig. 17.1) following occlusion of a branch of the middle cerebral artery. The signs are contralateral to the lesion: hemiplegia (arm > leg), hemisensory loss, upper motor neurone facial weakness and hemianopia. Initially the patient has a hypotonic hemiplegia with decreased reflexes; within days this develops into a spastic hemiplegia with increased reflexes and an extensor plantar response, i.e. an upper motor neurone lesion (Table 17.4). Weakness may recover gradually over days or months. Lacunar infarcts are small infarcts that produce localized deficits, e.g. pure motor stroke, pure sens-ory stroke.

Brainstem infarction Brainstem infarction causes complex patterns of dysfunction depending on the sites involved:

■ The lateral medullary syndrome, the most common of the brainstem vascular syndromes, is caused by occlusion of the posterior inferior cerebellar artery. It presents with sudden vomiting and vertigo, ipsilateral

Fig. 17.9 The arterial supply to the brain. (A) The area above the dotted line is supplied by the internal carotid artery and the area below the line is supplied by the vertebral artery. (B) A coronal section through the brain. The anterior cerebral artery supplies the medial surface of the hemisphere and the middle cerebral artery supplies the lateral surface of the hemisphere, including the internal capsule.

Horner's syndrome, facial numbness, cerebellar signs and palatal paralysis with a diminished gag reflex. On the side opposite the lesion there is loss of pain and temperature sensation.

■ Coma as a result of involvement of the reticular activating system.

■ The locked-in syndrome in which all voluntary muscles are paralysed except for those that control eye movement is caused by upper brainstem infarction

■ Pseudobulbar palsy (p. 736) is caused by lower brainstem infarction.

Multi-infarct dementia (vascular dementia) is a syndrome caused by mul-tiple small cortical infarcts, resulting in generalized intellectual loss; there is a stepwise progression with each infarct. The final picture is of dementia, pseudobulbar palsy and a shuffling gait resembling Parkinson's disease.

Management

Stroke is a medical emergency - ‘time lost is brain lost'. Immediate manage-ment is summarized in Emergency Box 17.1. Patients with a cerebellar infarct causing hydrocephalus or a large cerebral infarct with brain oedema and a risk of brain herniation should be referred for immediate neurosurgical evaluation.

Emergency Box 17.1

Immediate management of acute stroke

Investigations

• Brain CT (or MRI). Demonstrates the site of the lesion; distinguishes between ischaemic/haemorrhagic stroke; identiíies conditions mimicking stroke, e.g. cerebral tumour or abscess. Imaging is performed immediately (at the next scanning slot) in the following circumstances:

• patient presents within the time frame for thrombolysis

• early anticoagulation is indicated

• recent history of head injury

• severe headache at onset of stroke symptoms

• patient is taking anticoagulant treatment or has a known bleeding tendency

• depressed level of consciousness (Glasgow coma score <13). Otherwise brain imaging is performed within 24 hours of onset of symptoms. MRI is indicated if the underlying pathology is uncertain, the diagnosis is in doubt (CT may not show an infarct in the first few hours), or imaging is delayed for more than 10 days after stroke.

• Blood tests are similar to TIA (p. 745).

• ECG: to look for atrial fibrillation, myocardial infarction.

Treatment

• Aspirin. Aspirin 300 mg daily (orally, via nasogastric tube or rectally) should be given as soon as possible after the onset of stroke symptoms once a diagnosis of primary intracerebral haemorrhage has been excluded by brain imaging.

• Thrombolysis. Intravenous alteplase (tPA, p. 248) improves functional outcome if given within 4.5 hours of the onset of symptoms in acute ischaemic stroke. It is given immediately haemorrhage has been excluded in the emergency department provided that patients can be managed in an acute stroke Service with appropriate support from a stroke physician. Contraindications are listed on page 248.

• Hypertension. Blood pressure should only be lowered in the acute phase where there are likely to be complications of hypertension such as hypertensive encephalopathy, heart failure, or aortic dissection.

Supportive care

• Stroke unit. Dedicated stroke units improve outcome compared to management on a general ward.

• Swallowing and teeding. Dysphagia is common and may cause aspiration pneumonia and nutritional deíicit. Formal assessment of swallowing by trained staff is performed on admission and if the admission screen indicates swallowing problems specialist assessment (Speech and Language Therapy, SALT) is made within 24-72 hours. Feeding by fine-bore nasogastric tube or percutaneous gastrostomy may be necessary.

• Unconscious patient. Maintenance of hydration, frequent turning to avoid pressure sores and other supportive measures.

• Prevention of deep venous thrombosis by TED stockings. Heparin is not given.

Detailed clotting studies and autoantibody screen to look for evidence of conditions associated with thrombophilia (see Table 5.17) are indicated in younger patients with unexplained stroke. Echocardiography (in suspected cardioembolic stroke) and syphilis serology are performed in selected patients. Anticoagulation is given immediately for cerebral venous thrombosis but delayed for 14 days after the onset of ischaemic stroke in atrial fibrillation due to the risk of bleeding into the infarcted area. Carotid artery imaging, antithrombotic treatment and secondary prevention is similar to TIA (p. 746). Internal carotid endarterectomy or stenting reduces the risk of recurrent stroke (by 75%) in patients who have had an infarct and who have internal carotid artery stenosis which narrows the arterial lumen by more than 70%. It is considered in patients with a non-disabling stroke who are likely to have some recoverable function.

Further management of the stroke patient centres on identification and treatment of risk factors (p. 744) and rehabilitation to restore function. Optimal care is on a stroke rehabilitation unit that provides multidisciplinary services, coordinates disability-related medical care and trains caregivers. Physiotherapy is particularly useful in the first few months in reducing spas-ticity, relieving contractures and teaching patients to use walking aids. Fol-lowing recovery, the occupational therapist plays a valuable role in assessing the requirement for and arranging the provision of various aids and modifications in the home, such as stair rails, hoists, or wheelchairs. Patients and relatives may gain useful information and support from a Stroke Associa-tion (e.g. http://www.stroke.org.uk).

Prognosis

About one-quarter of patients will die in the first 2 years following a stroke; the prognosis is worse for bleeds than for infarction. Gradual improvement usually follows stroke, with a plateau reached 3-4 months after stroke onset, although one-third of long-term survivors are permanently dependent on the help of others. Only 25% of patients return to a level of everyday participation and physical functioning of community-matched persons who have not had a stroke. About 10% of all patients will suffer a recurrent stroke within 1 year.

Primary intracranial haemorrhage

Intracerebral haemorrhage

Major risk factors for intracerebral haemorrhage are hypertension, excess alcohol consumption, increasing age and smoking. These risk factors lead to secondary vascular changes such as small vessel disease and arterial aneu-rysms which may eventually rupture and bleed. Presentation is with sudden loss of consciousness and stroke (see above) often accompanied by a severe headache. Diagnosis is made on brain imaging by CT or MRI. Anticoagulants should be stopped in patients with intracerebral haemorrhage and the effects reversed by prothrombin complex concentrate. A decision to restart anti-coagulants (usually stopped for 7-10 days after an intracerebral haemor-rhage) is made on case by case basis. Patients with a large intracerebral haematoma causing deepening coma or brainstem compression or patients with a cerebellar bleed causing hydrocephalus as a result of obstruction of the drainage pathways for CSF fluid should be referred for immediate neu-rosurgical evaluation.

Subarachnoid haemorrhage (SAH)

Subarachnoid haemorrhage means spontaneous rather than traumatic arterial bleeding into the subarachnoid space.

Incidence

SAH accounts for 5% of strokes and has an annual incidence of 6 per 100 000. The mean age of patients at presentation is 50 years.

Aetiology

SAH is caused by rupture of:

■ Saccular (‘berry') aneurysms in 70% of cases. These are acquired lesions that are most commonly located at the branching points (Fig. 17.10) of

Fig. 17.10 The main cerebral arteries showing the circle of Willis and the most common sites for berry aneurysms. Frequency of occurrence, a-e (decreasing order): a, anterior communicating artery; b, origin of the posterior communicating artery; c, trifurcation of the middle cerebral artery; d, termination of the internal carotid artery; e, basilar artery.

the major arteries coursing through the subarachnoid space at the base of the brain (the circle of Willis).

■ Congenital arteriovenous malformations in 10%.

In 20% of cases no lesion can be found.

Clinical features

Most intracranial aneurysms remain asymptomatic until they rupture and cause a SAH. Some, however, become symptomatic because of a mass effect, and the most common symptom is a painful third-nerve palsy (p. 731). The typical presentation of SAH is the sudden onset of severe headache, often occipital, that reaches maximum intensity immediately or within minutes. The headache is typically described as the ‘worst ever' and there is absence of similar headaches in the past. It is often accompanied by nausea and vomiting, and sometimes loss of consciousness. On examination there may be signs of meningeal irritation (neck stiffness and a positive Kernig's sign), focal neurological signs and subhyaloid haemorrhages (between the retina and vitreous membrane) with or without papilloedema. Some patients have experienced small warning headaches a few days before the major bleed.

Investigation

■ CT scan is the investigation of choice and should be undertaken as soon as possible. It shows subarachnoid or intraventricular blood in 95% of cases undergoing scanning within 24 hours of the haemorrhage; the sensitivity decreases after that time.

■ Lumbar puncture (LP, p. 737) is indicated if there is a strong clinical suspicion of a SAH but the CT scan is normal. An increase in pigments (bilirubin and/or oxyhaemoglobin released from lysis and phagocytosis of red blood cells) is the key finding which supports the diagnosis of SAH. LP must be performed at least 12 hours after symptom onset to allow sufficient time for haemoglobin to degrade into oxyhaemoglobin and bilirubin. Detection of oxyhaemoglobin without bilirubin makes SAH less likely. Pigments in the CSF are detected by spectrophotometry of the supernatant after centrifugation of the last fraction of CSF taken at lumbar puncture. The specimen should be protected from light. Bilirubin can be detected in the CSF for up to 2 weeks after SAH.

■ MR angiography is usually performed to establish the source of bleeding in all patients potentially fit for surgery.

Management

Immediate management consists of bed rest and supportive measures with cautious control of hypertension. Nimodipine, a calcium-channel blocker, is given by mouth (60 mg 4-hourly) or by intravenous infusion (1-2 mg per hour via a Central line) to reduce cerebral artery spasm, a cause of ischaemia and further neurological deterioration. Hyponatraemia (which contributes to delayed cerebral ischaemia) occurs due to urinary salt loss and patients may require large volumes of intravenous 0.9% saline to maintain normal sodium concentrations. All patients should be discussed with a neurosurgeon. Oblit-eration of the aneurysm by surgical clipping or insertion of a fine wire coil under radiological guidance prevents rebleeding. Surviving patients should be advised on secondary prevention, especially on treatment of hypertension and the need to stop smoking.

Prognosis

Approximately 50% of patients die suddenly or soon after the haemorrhage. A further 10-20% die in the early weeks in hospital from further bleeding. The outcome is variable in the survivors; some patients are left with major neurological deficits. Glasgow coma score on admission has the most prog-nostic significance; patients with a score >12 usually have a good outcome.

Subdural haematoma (SDH)

SDH means accumulation of blood in the subdural space following the rupture of a vein running from the hemisphere to the sagittal sinus. It is almost always the result of head injury, often minor, and the latent interval between injury and symptoms may be weeks or months. Elderly patients and alcoholics are particularly susceptible because they are accident prone and their atrophic brains make the connecting veins more susceptible to rupture. The main clinical symptoms are headache, drowsiness and confusion, which may fluctuate. The diagnosis is usually made on CT, and treatment is by surgical removal of the haematoma.

Extradural haemorrhage

Extradural haematomas are caused by injuries that fracture the temporal bone and rupture the underlying middle meningeal artery. Clinically there is the picture of a head injury with a brief period of unconsciousness followed by a lucid interval of recovery. This is then followed by rapid deterioration with focal neurological signs and deterioration in conscious level if surgical drainage is not immediately carried out.

Ebook Essentials of Kumar and Clark's Clinical Medicine, 5e

1. Ethics and communication

Ethics and communication

2. Infectious diseases

Infectious diseases

3. Gastroenterology and nutrition

Gastroenterology and nutrition

4. Liver, biliary tract and pancreatic disease

Liver, biliary tract and pancreatic disease
LIVER BIOCHEMISTRY AND LIVER FUNCTION TESTS
SYMPTOMS AND SIGNS OF LIVER DISEASE
JAUNDICE
HEPATITIS
NON - ALCOHOLIC FATTY LIVER DISEASE (NAFLD)
CIRRHOSIS
COMPLICATIONS AND EFFECTS OF CIRRHOSIS
LIVER TRANSPLANTATION
TYPES OF CHRONIC LIVER DISEASE AND CIRRHOSIS
PRIMARY SCLEROSING CHOLANGITIS
BUDD - CHIARI SYNDROME
LIVER ABSCESS
LIVER DISEASE IN PREGNANCY
LIVER TUMOURS
GALLSTONES
THE PANCREAS
CARCINOMA OF THE PANCREAS
NEUROENDOCRINE TUMOURS OF THE PANCREAS

5. Haematological disease

Haematological disease
ANAEMIA
Assessment and treatment of suspected neutropenic sepsis
HAEMOLYTIC ANAEMIA
INHERITED HAEMOLYTIC ANAEMIAS
ACQUIRED HAEMOLYTIC ANAEMIA
MYELOPROLIFERATIVE DISORDERS
THE SPLEEN
BLOOD TRANSFUSION
THE WHITE CELL
HAEMOSTASIS AND THROMBOSIS
THROMBOSIS
THERAPEUTICS

6. Malignant disease

Malignant disease
MYELOABLATIVE THERAPY AND HAEMOPOIETIC STEM CELL TRANSPLANTATION
THE LYMPHOMAS
THE PARAPROTEINAEMIAS
PALLIATIVE MEDICINE AND SYMPTOM CONTROL

7. Rheumatology

Rheumatology
COMMON INVESTIGATIONS IN MUSCULOSKELETAL DISEASE
COMMON REGIONAL MUSCULOSKELETAL PROBLEMS
BACK PAIN
OSTEOARTHRITIS
INFLAMMATORY ARTHRITIS
THE SERONEGATIVE SPONDYLOARTHROPATHIES
Clinical features, Investigations
INFECTION OF JOINTS AND BONES
AUTOIMMUNE RHEUMATIC DISEASES
SYSTEMIC INFLAMMATORY VASCULITIS
DISEASES OF BONE
THERAPEUTICS

8. Water, electrolytes and acid–base balance

WATER AND ELECTROLYTE REQUIREMENTS
BODY FLUID COMPARTMENTS
REGULATION OF BODY FLUID HOMEOSTASIS
PLASMA OSMOLALITY AND DISORDERS OF SODIUM REGULATION
DISORDERS OF POTASSIUM REGULATION
DISORDERS OF MAGNESIUM REGULATION
DISORDERS OF ACID - BASE BALANCE
THERAPEUTICS

9. Renal disease

Renal disease
INVESTIGATION OF RENAL DISEASE
GLOMERULAR DISEASES
NEPHROTIC SYNDROME
URINARY TRACT INFECTION
TUBULOINTERSTITIAL NEPHRITIS
HYPERTENSION AND THE KIDNEY
RENAL CALCULI AND NEPHROCALCINOSIS
URINARY TRACT OBSTRUCTION
ACUTE RENAL FAILURE/ACUTE KIDNEY INJURY
CHRONIC KIDNEY DISEASE
RENAL REPLACEMENT THERAPY
CYSTIC RENAL DISEASE
TUMOURS OF THE KIDNEY AND GENITOURINARY TRACT
DISEASES OF THE PROSTATE GLAND
TESTICULAR TUMOUR
URINARY INCONTINENCE

10. Cardiovascular disease

COMMON PRESENTING SYMPTOMS OF HEART DISEASE
INVESTIGATIONS IN CARDIAC DISEASE
CARDIAC ARRHYTHMIAS
HEART FAILURE
ISCHAEMIC HEART DISEASE
RHEUMATIC FEVER
VALVULAR HEART DISEASE
PULMONARY HEART DISEASE
MYOCARDIAL DISEASE
CARDIOMYOPATHY
PERICARDIAL DISEASE
SYSTEMIC HYPERTENSION
ARTERIAL AND VENOUS DISEASE
ELECTRICAL CARDIOVERSION
DRUGS FOR ARRHYTHMIAS
DRUGS FOR HEART FAILURE
DRUGS AFFECTING THE RENIN - ANGIOTENSIN SYSTEM
NITRATES, CALCIUM - CHANNEL BLOCKERS AND POTASSIUM - CHANNEL ACTIVATORS

11. Respiratory disease


Respiratory disease
TUBERCULOSISnd
DIFFUSE DISEASES OF THE LUNG PARENCHYMA
OCCUPATIONAL LUNG DISEASE
CARCINOMA OF THE LUNG
DISEASES OF THE CHEST WALL AND PLEURA
DISORDERS OF THE DIAPHRAGM

12. Intensive care medicine

Intensive care medicine

13. Drug therapy, poisoning, and alcohol misuse

Drug therapy, poisoning, and alcohol misuse

14. Endocrine disease

Endocrine disease
PITUITARY HYPERSECRETION SYNDROMES
THE THYROID AXIS
MALE REPRODUCTION AND SEX
FEMALE REPRODUCTION AND SEX
THE GLUCOCORTICOID AXIS
THE THIRST AXIS
DISORDERS OF CALCIUM METABOLISM
DISORDERS OF PHOSPHATE CONCENTRATION
ENDOCRINOLOGY OF BLOOD PRESSURE CONTROL
DISORDERS OF TEMPERATURE REGULATION
THERAPEUTICS

15. Diabetes mellitus and other disorders of metabolism

DIABETES MELLITUS
DIABETIC METABOLIC EMERGENCIES
COMPLICATIONS OF DIABETES
SPECIAL SITUATIONS
HYPOGLYCAEMIA IN THE NON - DIABETIC
DISORDERS OF LIPID METABOLISM
THE PORPHYRIAS

16. The special senses

THE EAR
THE NOSE AND NASAL CAVITY
THE THROAT
THE EYE

17. Neurology

COMMON NEUROLOGICAL SYMPTOMS
COORDINATION OF MOVEMENT
THE CRANIAL NERVES
COMMON INVESTIGATIONS IN NEUROLOGICAL DISEASE
UNCONSCIOUSNESS AND COMA
STROKE AND CEREBROVASCULAR DISEASE
EPILEPSY AND LOSS OF CONSCIOUSNESS
NERVOUS SYSTEM INFECTION AND INFLAMMATION
HYDROCEPHALUS
HEADACHE, MIGRAINE AND FACIAL PAIN
SPINAL CORD DISEASE
DEGENERATIVE NEURONAL DISEASES
DISEASES OF THE PERIPHERAL NERVES
MUSCLE DISEASES
MYOTONIAS
DELIRIUM
THERAPEUTICS

18. Dermatology

Dermatology

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