EPILEPSY AND LOSS OF CONSCIOUSNESS

Epilepsy

A seizure is a convulsion or transient abnormal event caused by a paroxysmal discharge of cerebral neurones. Epilepsy is the continuing tendency to have such seizures. Epilepsy is common, with 2% of the UK population having two or more seizures during their lives, and in 0.5% epilepsy is an active problem.

Classification

Seizures are classified clinically as partial or generalized (Table 17.10). Partial seizures involve only a portion of the brain at their onset (e.g. temporal lobe), although these may later become generalized (secondarily generalized tonic-clonic seizures):

■ Generalized tonic-clonic seizures (grand mal seizures). There is a sudden onset of a rigid tonic phase followed by a convulsion (clonic phase) in which the muscles jerk rhythmically. The episode lasts typically for seconds to minutes, may be associated with tongue biting and inconti-nence of urine, and is followed by a period of drowsiness or coma for several hours.

■ Typical absence seizures (petit mal). This is usually a disorder of child-hood in which the child ceases activity, stares and pales for a few seconds only. It is characterized by 3-Hz spike and wave activity on the electroencephalogram (EEG). Children with petit mal tend to develop generalized tonic-clonic seizures in adult life.

■ Myoclonic, tonic and akinetic seizures There is isolated muscle jerking (myoclonic), intense stiffening of the body (tonic) or cessation of move-ment, falling and loss of consciousness (akinetic).

Table 17.10 The commoner types of seizure Generalized seizure types
Generalized seizure types
Bilateral abnormal electrical activity with bilateral motor manifestations and impaired
consciousness
Absence seizures (petit mal)
Generalised tonic–clonic seizures (grand mal)
Myoclonic seizures
Tonic seizures
Akinetic seizures
Partial seizure types
Electrical activity starts in one area of the brain
Simple partial seizures (without impaired awareness, e.g. Jacksonian seizures)
Complex partial seizures (with impaired awareness)
Partial seizures evolving to tonic–clonic seizures
Apparent generalized tonic–clonic seizures, with ECG but not clinical evidence of focal onset
Unclassifiable seizures
Seizures that do not fit a category above

■ Partial seizures involve epiletic activity in a part of the brain and are simple (not affecting consciousness or memory) or complex (affecting awareness or memory before, during or immediately after the seizure). Patients with focal seizures have symptoms depending on the area of the brain where the seizure starts, often the temporal lobe. The seizures may become generalized to affect the whole brain (secondary generalization). Jacksonian (motor) seizures originate in the motor cortex. They typically result in jerking movements, typically beginning in the corner of the mouth or thumb and index finger, and spreading to involve the limbs on the opposite side of the epileptic focus. Paralysis of the involved limbs may follow for several hours (Todd's paralysis). Temporal lobe seizures are associated with olfactory and visual hallucinations, blank staring, feelings of unreality (jamais-vu) or undue familiarity (déjà-vu) with the surroundings.

Aetiology and precipitants

Flashing lights or a flickering television screen may provoke an attack in susceptible patients. A cause for epilepsy is found in less than one-third of cases in UK surveys. Known causes include cerebrovascular disease (15%), cerebral tumours (6%), alcohol-related seizures (6%), post-traumatic epi-lepsy (2%) and other rarer intracerebral causes. Occasionally, metabolic disturbances such as hypoglycaemia, acute hypoxia, hypocalcaemia, hyponatraemia, uraemia and hepatocellular failure present with convulsions.

About 30% of patients have a first-degree relative with epilepsy, although the exact mode of inheritance is unknown. Primary epilepsies are due to complex developmental abnormalities of neuronal control; there are abnormalities in synaptic connections and distribution and release of neurotransmitters.

Evaluation and investigation

There are three steps in the evaluation of a patient with possible epilepsy:

1. Confirm if the patient has epilepsy. The diagnosis is made clinically and a detailed description of the attack from an eye-witness is invaluable. Disorders causing attacks of altered consciousness must be differenti-ated from epilepsy (Table 17.3).

2. Determine the patient's seizure type (see classification).

3. Identify any underlying cause for epilepsy:

■ The electroencephalogram (EEG) is used to assist in the classification of epilepsy and to confirm the clinical suspicion. It is frequently normal between attacks and false positive ‘non-specific' abnormali-ties may be present in non-epileptics. During a seizure the EEG is almost always abnormal and is shown typically by a cortical spike focus (e.g. in a temporal lobe) or by generalized spike and wave activity. Video-EEG recording is used where the diagnosis of epilepsy is in doubt.

■ Brain imaging is indicated in all new cases to exclude an underlying lesion. CT is used in the emergency setting to look for a space occu-pying lesion, e.g. tumour. MRI with imaging of the hippocampi is used routinely to study epilepsy.

Management

Emergency measures

The emergency treatment is to ensure that patients harm themselves as little as possible and that the airway remains patent. Most seizures stop spontane-ously. A prolonged seizure (longer than 3 minutes) or repeated seizures are treated with rectal (10 mg) or i.v. diazepam or lorazepam. Repeated seizures with brief periods of recovery may lead to status epilepticus.

Status epilepticus This is a medical emergency. There are continuous seizures without recovery of consciousness. When grand mal seizures follow one another, there is a risk of death from cardiorespiratory failure. Precipitat-ing factors in a known epileptic include abruptly stopping antiepileptic treat-ment, intercurrent illness, alcohol abuse and poor compliance with therapy; over 50% of all episodes occur in patients without any history of epilepsy. Rectal diazepam or buccal midazolam (10 mg) is given out of hospital.

Management in hospital is summarized in Emergency Box 17.2. EEG monitor-ing in refractory status or diagnosis in doubt (consider pseudostatus - non-epileptic attacks with a psychological basis). Once status is controlled regular anticonvulsant therapy is continued to prevent subsequent fits. Intravenous treatment is withdrawn when anticonvulsant therapy is established.

Antiepileptic drugs (AEDs)

AEDs are indicated when there is a firm clinical diagnosis of recurrent sei-zures or after a first seizure with features associated with a high risk of seizure recurrence (abnormal EEG and/or structural brain abnormality on imaging). Treatment is started with a single first-line antiepileptic drug (Table 17.11). Monotherapy is the aim and the dose is increased until seizure control is achieved or tolerance exceeded. Routine measurement of serum drug

Emergency Box 17.2
Management and investigation of status epilepticus
General measures
• Administer oxygen
• Secure venous access via a large vein; many anticonvulsants cause phlebitis
• Cardiorespiratory monitoring and pulse oximetry
• Thiamine, 250 mg i.v. over 10 minutes, if nutrition poor or alcohol abuse suspected. In the UK give Vitamin B and C, high-potency ampoules, one pair i.v. over 10 minutes.
Control of seizures
First line. Lorazepam 4 mg i.v. at 2 mg/min, repeated after 10 minutes if no response. Give rectal diazepam (10–20 mg) if no intravenous access. Lorazepam may cause respiratory depression and hypotension, and facilities for resuscitation should be available.
Second line. If seizures continue, give phenytoin 18 mg/kg i.v. 50 mg/min or fosphenytoin (p. 800). Both may cause cardiac dysrhythmias, and ECG monitoring is necessary.
Third line. Phenobarbital 15 mg/kg at a rate not exceeding 100 mg/min and repeated at intervals of 6–8 hours if necessary. If seizures continue despite these measures, use tiopental or propofol general anaesthesia with assisted ventilation.
Investigations
• Urgent: blood glucose, serum electrolytes including calcium and magnesium, drug screen, anticonvulsant levels
• Consider brain CT scan, lumbar puncture and blood cultures, depending on clinical circumstances.

Table 17.11 First-line treatment depending on seizure type

Seizure type

Drug

Major side-effects of drug treatment

Generalized tonic—clonic

Sodium valproate+

Weight gain, hair loss, liver damage, blood dyscrasias

Lamotrigine

TEN

Carbamazepine

Rashes, leucopenia, TEN

Topiramate

Weight loss, renal stones, glaucoma

Phenytoin*

Rashes, blood dyscrasias, lymphadenopathy, SLE, TEN, gum hypertrophy, hirsuitism

Petit mal

Sodium valproate†

Ethosuximide

Rashes, blood dyscrasias, night terrors

Partial seizures

Lamotrigine
Carbamazepine

 

Sodium valproate
Phenytoin*

*in developing countries; TEN, toxic epidermal necrolyis; SLE, systemic lupus
erythematosus.
†avoid in women of childbearing age; associated with highest risk of major congenital
malformation in fetuses exposed to drug during pregnancy.

levels is necessary only for phenytoin and phenobarbital. Levels should also be measured if non-compliance is suspected or if there are signs of toxicity. Idiosyncratic side-effects (i.e. non-dose related), which tend to be more common than dose-related effects, are listed in Table 17.11. Intoxication with all anticonvulsants causes a syndrome of ataxia, nystagmus and dysarthria. Side-effects of chronic administration of phenytoin (gum hypertrophy, hyper-trichosis, osteomalacia and folate deficiency) are reduced by maintaining serum levels within the therapeutic range. Phenytoin is a potent hepatic enzyme inducer and will reduce the efficacy of the contraceptive pill. Many new drugs have been developed and there remain different views about the most appropriate drugs for each seizure type.

Drug withdrawal Gradual withdrawal of drugs should only be undertaken when the patient has been seizure-free for at least 2 years, and is only achieved successfully in less than 50%. Many patients will have further fits, resulting in a threat to employment and driving (see below).

Neurosurgical treatment

Surgical treatment, e.g. amputation of the anterior temporal lobe, cures epilepsy in 50% of patients with poorly controlled epilepsy and a clearly defined focus of abnormal electrical activity (<1% of all patients with epilepsy).

Advice to patients

Patients should restrict their lives as little as possible but follow simple advice, e.g. avoid swimming alone, avoid dangerous sports, such as rock climbing, leave the door open when taking a bath. In European Union member states, patients with epilepsy (whether on or off treatment) may drive a motor vehicle (cars, vans, motorcycles) provided that they have been seizure-free for a year. Patients who wish to drive heavy goods vehicles (buses, lorries, etc.) must have been seizure-free and off all anti-epileptic drugs for 10 years or more.

MOVEMENT DISORDERS

The extrapyramidal system is a general term for the basal ganglia and their connections with other brain areas, particularly those concerned with move-ment. The overall function of this system is the initiation and modulation of movement. Extrapyramidal or movement disorders are:

■ Akinetic-rigid syndromes, i.e. slowed movement with increased muscle tone

■ Dyskinesias - added uncontrollable movements.

Table 17.12 Movement disorders
Akinetic–rigid syndromes
Idiopathic Parkinson’s disease
Drug-induced parkinsonism, e.g. phenothiazines
MPTP-induced parkinsonism
Postencephalitic parkinsonism
‘Parkinsonism plus’
Wilson’s disease
Childhood akinetic–rigid syndromes
Dyskinesias
Essential tremor
Chorea
Hemiballismus
Myoclonus
Tics
Dystonias
Paroxysmal dyskinesias
MPTP, methylphenyltetrahydroyridine

Akinetic-rigid syndromes

Idiopathic Parkinson’s disease

Parkinson's disease (PD) is a common neurodegenerative disease developing predominantly in older people. The clinical features principally result from the progressive depletion of dopamine-secreting cells in the substantia nigra. These neurones project to the striatum and their loss leads to alteration in activity of the neural circuits within the basal ganglia that regulate movement. Disruption of dopamine along the non-striatal pathways accounts for the neuropsychiatric pathology associated with PD. Cell loss in PD is thought to be due to abnormal accumulation of alpha-synuclein bound to ubiquitin which forms cytoplasmic inclusions called Lewy bodies.

Aetiology

The cause of the disease is unknown. Factors possibly involved are:

■ MPTP (methylphenyl-tetrahydropyridine) an impurity produced during illegal synthesis of opiates produces severe parkinsonism.

■ Survivors of an epidemic of encephalitis lethargica in the early 20th century developed parkinsonism. However, there is no evidence that idiopathic PD is caused by an environmental toxin or an infective agent.

■ Parkinson's disease is less prevalent in tobacco smokers than in lifelong abstainers.

■ Genetic factors. There is clustering of early-onset PD is some families. Mutations in the Parkin gene, a-synuclein gene and ubiquitin caroxyl-terminal hydrolase L1 gene have been found in some of these families. Relevance to the common sporadic older PD cases is unclear.

Clinical teatures

The combination of rest tremor, rigidity and bradykinesia (slow movements) develops over months or several years together with changes in posture. These features are initially more prominent on one side:

■ Tremor. This is a characteristic 4-7 Hz resting tremor (cf. cerebellar disease), usually most obvious in the hands (‘pill-rolling' of the thumb and fingers), improved by voluntary movement and made worse by anxiety.

■ Rigidity refers to the increase in tone in the limbs and trunk. The limbs resist passive extension throughout movement (lead pipe rigidity, or cogwheel when combined with tremor), in contrast to the hypertonia of an upper motor neurone lesion (p. 720), where resistance falls away as the movement continues (clasp-knife).

■ Akinesia (poverty of movement) There is difficulty in initiating move-ment (starting to walk, or rising from a chair). The face is expressionless and unblinking. Speech is slow and monotonous. The writing becomes small (micrographia) and tends to tail off at the end of a line.

■ Posturalchanges. A stoop is characteristic. The gait is shuffling, festinant (hurrying) and with poor arm swinging. The posture is sometimes called ‘simian', to describe the forward flexion, immobility of the arms and lack of facial expression. Balance is poor, with a tendency to fall.

Non-motor features may predate motor features and consist of neuropsychi-atric symptoms (depression, hallucinations, dementia, impulsive behaviours), sleep disorders (insomnia, sleep fragmentation, vivid dreams), gastrointesti-nal and autonomic disorders (drooling of saliva, excess sweating, dysphagia, constipation) and fatigue and weight loss. There is gradual progression of the disease over 10-15 years, with death resulting most commonly from bronchopneumonia.

Investigations

The diagnosis is clinical. Other brain diseases (e.g. multi-infarct dementia, repeated head injury) can causes features of parkinsonism, i.e. slowing, rigidity and tremor, which can usually be differentiated from idiopathic PD on clinical grounds; brain imaging (MRI or CT) is sometimes needed

Management

The decision to start treatment is determined by the degree to which the patient is functionally impaired. Treatment does not alter the natural history. Intial therapy is with one of:

Levodopa (L-dopa, a dopamine precursor) with a peripheral dopa-decarboxylase inhibitor - benserazide or carbidopa. This combined therapy reduces the peripheral side-effects, principally nausea, of L-dopa and its metabolites. Over the years, therapy may become less effective, even with increasing doses. Patients may also switch between periods of dopamine-induced dyskinesias (choreas and dystonic movements) and periods of immo-bility (‘on-off' syndrome).

Dopamine agonists are non-ergot dopamine agonists (ropinirole, prami-pexole, rotigotine). Possible side-effects are impulse control disorders (pathological gambling, compulsive shopping, hypersexuality) and excessive daytime sleepiness.

Monoamine oxidase B inhibitor (e.g. selegiline) inhibits the catabolism of dopamine in the brain.

The options for managing disease progression and the loss of smooth motor control associated with levodopa-based drugs are shortening the inter-val between drug dosing and increasing the dose, adding or swapping to other antiparkinsonian drugs (see above), using catechol-O-methyl trans-ferase inhibitors (entacapone, tolcapone) to prevent peripheral breakdown of L-dopa or using apomorphine by subsutaneous pump.

Additional treatment Physiotherapy can improve gait and help to prevent falls. Selective serotonin reuptake inhibitors are the treatment of choice for depression. Stereotactic neurosurgery is occasionally used to reduce motor fluctuations and dyskinesia. Information and support for patients and relatives is provided by the Parkinson's Disease Society (http://www.parkinsons.org.uk).

Other akinetic-rigid syndromes

Drug-induced parkinsonism

Reserpine, phenothiazines and butyrophenones block dopamine receptors and may induce a parkinsonian syndrome with slowness and rigidity, but usually with little tremor. These syndromes tend not to progress, they respond poorly to L-dopa, and the correct management is to stop the offending drug.

‘Parkinsonism plus’

This describes rare disorders in which there is parkinsonism and evidence of a separate pathology. Progressive supranuclear palsy is the most common disorder and consists of axial rigidity, dementia and signs of parkinsonism, together with gaze paresis. Other examples are multiple system atrophy (early severe autonomic neuropathy), such as olivo-ponto-cerebellar degen-eration and primary autonomic failure (Shy-Drager syndrome). Unlike idipo-pathic PD, there is a poor response to L-dopa in these conditions.

Dyskinesias

Benign essential tremor

This is usually a familial (autosomal dominant) tremor of the arms and head (titubation) which occurs most frequently in elderly people. Unlike the tremor of Parkinson's disease it is not usually present at rest, but is most obvious when the hands adopt a posture such as holding a glass or a spoon (p. 759). It is made worse by anxiety and improved by alcohol, propranolol, primadone (an anticonvulsant), and mirtazapine (an antidepressant).

Chorea

Chorea is a continuous flow of jerky, quasi-purposive movements, flitting from one part of the body to another. They may interfere with voluntary movements but cease during sleep. The causes of chorea are listed in Table 17.13.

Huntington’s disease

This is a rare autosomal dominant condition with full penetrance. There is a relentlessly progressive course with chorea and personality change preceding dementia and death. Symptoms usually begin in middle age. Expansion of CAG repeats in the Huntington's disease gene on chromosome 4 leads to production of mutant huntingtin protein. It is not known how the mutant

Table 17.13 Causes of chorea
Huntington’s disease
Dentato-rubro-pallido-luysian atrophy
Sydenham’s chorea
Benign hereditary chorea
Drug induced: phenytoin, levodopa, alcohol
Thyrotoxicosis
Pregnancy and the oral contraceptive pill
Hypoparathyroidism
Systemic lupus erythematosus
Polycythaemia vera
Stroke (basal ganglia)
Other CNS disease: tumour, trauma subdural haematoma, following carbon monoxide poisoning, Wilson’s disease

protein causes disease. There is loss of neurones within the basal ganglia, leading to depletion of GABA (y-aminobutyric acid) and acetylcholine but sparing dopamine. No treatment arrests the disease, and the management is symptomatic treatment of chorea and genetic counselling of family members.

Hemiballismus

Hemiballismus (also called hemiballism) describes violent swinging move-ments of one side of the body, usually caused by infarction or haemorrhage in the contralateral subthalamic nucleus.

Myoclonus

Myoclonus is the sudden, involuntary jerking of a single muscle or group of muscles. The most common example is benign essential myoclonus, which is the sudden jerking of a limb or the body on falling asleep. Myoclonus also occurs with epilepsy and some encephalopathies.

Tics

Tics are brief, repeated stereotypical movements, usually involving the face and shoulders. Unlike other involuntary movements it is usually possible for the patient to control tics.

Dystonias

Dystonias are prolonged spasms of muscle contraction. They occur as a symptom of neurological disease, e.g. Wilson's disease, but are usually focal, of unknown cause and occur without other neurological problems, e.g. blepharospasm (spasms of forced blinking) or spasmodic torticollis (the head is turned and held to one side or drawn backwards or forwards). Targeted injection of minute amounts of botulinum toxin (which inhibits the release of acetylcholine from nerve endings) into the muscle provides temporary relief. Acute dystonic reactions are seen with phenothiazines, butyrophenones and metoclopramide, and can occur after a single dose of the drug. Spasmodic torticollis, trismus and oculogyric crises (i.e. episodes of sustained upward gaze) may occur. Acute dystonias respond promptly to an anticholinergic drug administered by intravenous or intramuscular injection, e.g. benzatropine (1-2 mg) or procyclidine (5 mg).

Multiple sclerosis (MS)

MS is a chronic debilitating autoimmune disorder of the central nervous system in which there are multiple plaques of demyelination within the brain and spinal cord. These plaques are disseminated both in time and place, hence the old name ‘disseminated sclerosis'.

Epidemiology

MS typically begins in early adulthood and the disease is more common in women. The prevalence varies widely (60 per 10 000 in England); it is rare in tropical countries.

Aetiology

Although the precise mechanism is unknown, there is an inflammatory process in the white matter of the brain and spinal cord mediated by B cells and CD4 T cells. It is thought that exposure to a specific infectious agent (Epstein-Barr virus, EBV) in childhood may predispose to the later develop-ment of MS in a genetically susceptible host. Antibodies produced by B cells and T cells directed against EBV nuclear antigens may be redirected to attack CNS myelin because of molecular mimicry.

Pathology

Inflammation, demyelination and axonal loss are the major feature of the MS plaque and cause the clinical manifestations. Plaques are perivenular and have a predilection for distinct CNS sites: optic nerves, periventricular white matter, brainstem and its cerebellar connections, and the cervical spinal cord (corticospinal tracts and posterior columns). The peripheral nerves are never affected.

Clinical features

The typical patient presents as a young adult (onset of MS rare before puberty or after 60 years) with two or more clinically distinct episodes of CNS dys-function followed by a remission during which symptoms and signs resolve to some extent within weeks. The regression of symptoms is attributed to the resolution of inflammatory oedema and to partial remyelination. Three characteristic common presentations of relapsing and remitting MS are optic neuropathy, brainstem demyelination and spinal cord lesions.

Optic neuropathy Inflammation of the optic nerve produces blurred vision and unilateral eye pain. A lesion in the optic nerve head produces disc swelling (optic neuritis) and pallor (optic atrophy) following the attack. When inflammation occurs in the optic nerve further away from the eye (retrobulbar neuritis) examination of the fundus is normal.

Brainstem demyelination produces diplopia, vertigo, dysphagia and nystagmus.

Spinal cord lesions Sensory symptoms including numbness and pins and needles are common in MS and reflect spinothalamic and posterior column lesions. Spastic paraparesis is the result of plaques of demyelination in the cervical or thoracic cord.

In some patients there will only be one or two attacks with little residual neurological deficit, and they remain very well for years. At the other extreme, an increasing neurological deficit accumulates and spastic tetraparesis, ataxia, brainstem signs, blindness, incontinence and dementia characterize the final stages. Death follows from recurrent urinary tract infection, uraemia and bronchopneumonia.

Other less common clinical patterns of MS are primary progressive (disease progression from the onset with only occasional and minor improve-ments), secondary progressive (initial relapsing/remitting course followed by progression) and, occasionally, a fulminating course over some months (ful-minant MS).

Differential diagnosis

Initially, individual plaques (in the optic nerve, brainstem or cord) may cause diagnostic difficulty and must be distinguished from inflammatory (Behget's disease, systemic lupus erythematosus, sarcoid), mass or vascular lesions. A single lesion in the cord may produce paraparesis and a sensory level and mechanical cord compression (p. 779) must be excluded by MRI. In young patients with a relapsing and remitting course the diagnosis is straight-forward, as few other diseases produce this clinical picture.

Investigations

■ MRI of brain and spinal cord is the definitive investigation and shows plaques particularly in the periventricular area and brainstem. Lesions are rarely visible on CT.

■ Electrophysiological tests. Visual, auditory and somatosensory evoked potentials may be prolonged, even in the absence of any past or present visual symptoms.

■ CSF examination is usually unnecessary as the diagnosis is made with MRI or evoked potentials and a compatible clinical picture. Protein con-centration and cell count (5-60 mononuclear cells/mm3) are raised. CSF electrophoresis shows oligoclonal IgG bands in most cases but these are not specific.

Management

■ Short courses of steroids, e.g. i.v. methylprednisolone 1000 mg/day for 3 days, is used in relapses and may reduce severity. However, they do not influence long-term outlook.

■ Subcutaneous administration of β-interferon reduces the relapse rate by one-third in relapsing/remitting disease and may delay the time to severe debility. Treatment is prolonged, expensive and associated with side-effects, such as ‘flu-like symptoms'.

■ Glatiramer acetate is antigenically similar to myelin basic protein and competes with various myelin antigens for their presentation to T cells. It has similar efficacy to interferons and is given by subcutabneous injection.

■ Natalizumab and mitoxantrone are reserved as second line therapy due to side-effects (progressive multifocal leucoencephalopathy and cardiac toxicity respectively).

■ Physiotherapy and occupational therapy maintain the mobility of joints, and muscle relaxants (e.g. baclofen, dantrolene and benzodiazepines) reduce the discomfort and pain of spasticity. Multidisciplinary team liaison between patient, carers, medical practitioners and therapists is essential for any patient with chronic disabling disease. Urinary catheteri-zation is eventually needed for those with bladder involvement. The Multiple Sclerosis Society provides information and support for patients and relatives (http://www.mssociety.org.uk).

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

KEYWORD : Phác Đồ Chữa Bệnh, Bệnh Viện Bạch Mai, Từ Dũ , 115, Bình Dân, Chấn thương chỉnh hình, Chợ Rẫy, Đại học Y Dược, Nhân Dân Gia Định, Hoàn Mỹ, Viện Pasteur, Nhi Đồng Ung bướu, Quân Đội 103, 108,Phụ Sản Trung Ương, Bộ Y Tế,Phòng Khám, Hà Nội, Hải Dương, Thái Bình, Hồ Chí Minh, Sài Gòn, Đà Nẵng, Huế, Vinh, Đồng Nai, Bình Dương, Hải Phòng, Quảng Ninh, Hiệu Quả Cao, Chữa Tốt, Khỏi Bệnh, Là Gì, Nguyên Nhân, Triệu Chứng, Ăn Uống, Cách Chữa, Bài Thuốc
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