THE CRANIAL NERVES

The 12 cranial nerves and their nuclei are distributed approximately equally between the three brainstem segments (Fig. 17.4). The exceptions are the first and second cranial nerves (nerves I and II), whose neurones project to the cerebral cortex. In addition, the sensory nucleus of nerve V extends from the midbrain to the spinal cord, and the nuclei of nerves VII and VIII lie not only in the pons but also in the medulla.

The olfactory nerve (first cranial nerve)

The olfactory nerve subserves the sense of smell. The most common cause of anosmia (loss of the sense of smell) is simply nasal congestion. Neurological causes include tumours on the floor of the anterior fossa and head injury.

Fig. 17.4 The location of the cranial nerves and their nuclei within the midbrain, pons and medulla as seen laterally.

The optic nerve (second cranial nerve) and the visual system

The optic nerves enter the cranial cavity through the optic foramina and unite to form the optic chiasm, beyond which they are continued as the optic tracts. Fibres of the optic tract project to the visual cortex (via the lateral geniculate body) and the third nerve nucleus for pupillary light reflexes (Figs 17.5 and 17.6).

The assessment of optic nerve function includes measurement of visual acuity (using a Snellen test chart), colour vision (using Ishihara colour plates) and the visual fields (by confrontation and perimetry), and examination of the fundi with the ophthalmoscope. In addition the pupillary responses, mediated by both the optic and the oculomotor nerve (third cranial nerve), must be tested.

Visual field defects

There are three main types of visual field defects (Fig. 17.5):

■ Monocular, caused by damage to the eye or nerve

■ Bitemporal, resulting from lesions at the chiasm

1, Paracentral scotoma- retinal lesion.

2, Mononuclear field loss - optic nerve lesion.

3, Bitemporal hemianopia- chiasmal lesion.

4, Homonymous hemianopia- optic tract lesion.

5, Homonymous quadrantanopia- temporal lesion.

6, Homonymous quadrantanopia- parietal lesion.

7, Homonymous hemianopia- occipital corlex or optic radiation.

8, Homonymous hemianopia- occipital pole lesion.

Fig. 17.5 Diagram of the visual pathways demonstrating the main field defects. At the optic chiasm (3), fibres derived from the nasal half of the retina (the temporal visual field) decussate, whereas the fibres from the temporal half of the retina remain uncrossed. Thus the right optic tract (4) is composed of fibres from the right half of each retina which ‘see’ the left half of both visual fields. Lesions of the retina (1) produce scotoma (small areas of visual loss) or quadrantanopia. Lesion at 2 produces blindness in the right eye with loss of direct light reflex. Lesion at 3 produces bitemporal hemianopia. Lesions at 4, 5 and 6 produce homonymous hemianopia with macular involvement. Lesions at 7 and 8 produce homonymous hemianopia with macular sparing at 7.

Fig. 17.6 Pupillary light reflex.
Afferent pathway
(1) A retinal image generates action potentials in the optic nerve.
(2) These travel via axons, some of which decussate at the chiasm and pass
through the lateral geniculate bodies.
(3) Synapse at each pretectal nucleus.
Efferent pathway
(4) Action potentials then pass to each Edinger–Westphal nucleus of III,
(5) then, to the ciliary ganglion via the third nerve,
(6) leading to constriction of the pupil being illuminated (direct reflex) and, by
the consensual reflex, the contralateral pupil.

■ Homonymous hemianopia, caused by lesions in the tract, radiation, or a lesion in the visual cortex.

Optic nerve lesions Unilateral visual loss, starting as a central or para-central scotoma (an area of depressed Vision within the visual field), is characteristic of optic nerve lesions. Complete destruction of one optic nerve results in blindness in that eye and loss of the pupillary light reflex (direct and consensual). Optic nerve lesions result from demyelination (e.g. multiple sclerosis), nerve compression and occlusion of the retinal artery (e.g. in giant cell arteritis). Other causes include trauma, papilloedema, severe anaemia and drugs or toxins, e.g. ethambutol, quinine, tobacco and methyl alcohol.

Defects of the optic chiasm The most common cause of bitemporal hemianopia (i.e. blindness in the outer half of each visual field) is a pituitary adenoma, which compresses the decussating fibres from the nasal half of each eye. Other causes are craniopharyngioma and secondary neoplasm.

Defects of the optic tract and radiation Damage to the tracts or radiation, usually by tumour or a vascular accident, produces a homonymous hemianopia (blindness affecting either the right or the left half of each visual field) in one half of the visual field contralateral to the lesion.

Defects of the occipital cortex Homonymous hemianopic defects are caused by unilateral posterior cerebral artery infarction. The macular region may be spared in ischaemic lesions as a result of the dual blood supply to this area from the middle and posterior cerebral arteries. In contrast, injury to one occipital pole produces a bilateral macular (central) field defect.

Optic disc oedema (papilloedema) and optic atrophy

The principal pathological appearances of the visible part of the nerve, the disc, are:

■ Swelling (papilloedema)

■ Pallor (optic atrophy).

Papilloedema Papilloedema produces few visual symptoms in the early stages. As disc oedema develops there is enlargement of the blind spot and blurring of vision. The exception is optic neuritis, in which there is early and severe visual loss. The common causes of papilloedema are:

■ Raised intracranial pressure, e.g. from a tumour, an abscess or meningitis

■ Retinal vein obstruction (thrombosis or compression)

■ Optic neuritis (inflammation of the optic nerve, often caused by demyelination)

■ Accelerated hypertension.

Optic atrophy Optic atrophy is the end result of many processes that damage the nerve (see Optic nerve lesions, above). The degree of visual loss depends upon the underlying cause.

The pupils

The pupils constrict in response to bright light and convergence (when the centre of focus shifts from a distant to a near object). The parasympathetic efferents that control the constrictor muscle of the pupil arise in the Edinger-Westphal nucleus in the midbrain, and run with the oculomotor (third) nerve to the eye. The Edinger-Westphal nucleus receives afferents from the optic nerve (for the light reflex) and from the convergence centre in the midbrain (Fig. 17.6).

Sympathetic fibres which arise in the hypothalamus produce pupillary dilatation. They run from the hypothalamus through the brainstem and cervical cord and emerge from the spinal cord at T1. They then ascend in the neck as the cervical sympathetic chain, and travel with the carotid artery into the head.

The main causes of persistent pupillary dilatation are:

■ A third cranial nerve palsy (see later)

■ Antimuscarinic eyedrops (instilled to facilitate examination of the fundus)

■ The myotonic pupil (Holmes-Adie pupil): this is a dilated pupil seen most commonly in young women. There is absent (or much delayed) reaction to light and convergence. It is of no pathological significance and may be associated with absent tendon reflexes.

The main causes of persistent pupillary constriction are:

■ Parasympatheticomimetic eyedrops used in the treatment of glaucoma.

■ Horner’s syndrome, resulting from the interruption of sympathetic fibres to one eye. There is unilateral pupillary constriction, slight ptosis (sympathetic fibres innervate the levator palpebrae superioris), enoph-thalmos (backward displacement of the eyeball in the orbit) and loss of sweating on the ipsilateral side of the face. A lesion affecting any part of the sympathetic pathway to the eye results in a Horner’s syndrome. Causes include diseases of the cervical cord, e.g. syringomyelia, involve-ment of the T1 root by apical lung cancer (Pancoast’s tumour), and lesions in the neck, such as trauma, surgical resection or malignant lymph nodes.

■ Argyll Robertson pupil: this is the pupillary abnormality seen in neuro-syphilis and occasionally in diabetes mellitus. There is a small irregular pupil which is fixed to light but which constricts on convergence.

■ Opiate addiction.

Cranial nerves III-XII

The cranial nerves III-XII may be damaged by lesions in the brainstem or during their intracranial and extracranial course. The site of a lesion may be suggested if clinical examination shows the involvement of other cranial nerves at that site.

■ A seventh-nerve palsy, together with cerebellar signs and involvement of the fifth, sixth and eighth cranial nerves, suggests a lesion of the cere-bellopontine angle, commonly a meningioma or acoustic neuroma

■ An isolated seventh-nerve palsy in a patient with a parotid tumour sug-gests involvement during its extracranial course in the parotid

■ Cavernous sinus lesions (thrombosis, tumours, internal carotid artery aneurysm) involve the oculomotor nerves and the ophthalmic and some-times maxillary division of the fifth cranial nerve during their intracranial course

■ Conditions which can affect any cranial nerve are diabetes mellitus, sarcoidosis, vasculitis, syphilis and brainstem tumours, multiple sclerosis and infarction.

The ocular movements and the third, fourth and sixth cranial nerves

These three cranial nerves supply the six external ocular muscles, which move the eye in the orbit (Fig. 17.7). The abducens nerve (sixth cranial nerve) supplies the lateral rectus muscle and the trochlear (fourth cranial nerve) supplies the superior oblique muscle. All the other extraocular muscles, the sphincter pupillae (parasympathetic fibres) and the levator palpebrae sup-erioris are supplied by the oculomotor nerve (third cranial nerve). Normally the brainstem (with input from the cortex, cerebellum and vestibular nucleus) coordinates the functions of these three cranial nerves, so that eye movement is symmetrical (conjugate gaze). Thus infranuclear (lower motor neurone)

Fig. 17.7 The action of the external ocular muscles. The muscles of the eye move the eyeball in various directions. The lateral rectus muscle moves the eyeball to the temple, away from the midline of the face. The medial rectus muscle moves the eyeball to the nose, toward the midline of the face. The superior rectus muscle moves the eyeball upward, and the inferior rectus muscle moves the eyeball downward. The superior oblique muscle moves the eyeball downward and outward. The inferior oblique muscle moves the eyeball upward and outward.

lesions of the third, fourth and sixth cranial nerves lead to paralysis of individual muscles or muscle groups. Supranuclear (upper motor neurone) lesions, e.g. brainstem involvement by multiple sclerosis, lead to paralysis of conjugate movements of the eyes.

■ Oculomotor (third) nerve lesions cause unilateral complete ptosis, the eye faces ‘down and out', and the pupil is dilated and fixed to light and convergence. This is the picture of a complete third-nerve palsy, of which the most common cause is a ‘berry' aneurysm arising in the posterior communicating artery, which runs alongside the nerve. Frequently the lesion is partial, particularly in diabetes mellitus, when parasympathetic fibres are spared and the pupil reacts normally.

■ In lesions on the abducens (sixth) nerve the eye cannot be abducted beyond the midline. The unopposed pull of the medial rectus muscle causes the eye to turn inward, thereby producing a squint (squint, or strabismus, is the appearance of the eyes when the visual axes do not meet at the point of fixation). Patients complain of diplopia or double vision, which worsens when they attempt to gaze to the side of the lesion.

■ Trochlear nerve lesions in isolation are rare. The patient complains of diplopia when attempting to look down and away from the affected side.

Disordered ocular movements may also result from disease of the ocular muscles (e.g. muscular dystrophy, dystrophia myotonica) or of the neuromus-cular junction (e.g. myasthenia gravis). In these conditions all the muscles tend to be affected equally, presenting a generalized restriction of eye movements.

The trigeminal nerve (fifth cranial nerve)

The trigeminal nerve has both motor and sensory functions and enters the brainstem at the level of the pons. The neurones for pain and temperature descend to the upper cervical spine before they synapse with neurones of the descending tract of the fifth nerve. Second order neurones then cross over and ascend to the thalamus. The sensory portion of this nerve supplies sensation to the face and scalp as far back as the vertex through its three divisions (Fig. 17.8). It also supplies the mucous membranes of the sinuses, the nose, mouth, tongue and teeth. The motor root travels with the mandibu-lar division and supplies the muscles of mastication.

Diminution of the corneal reflex is often the first sign of a fifth-nerve lesion. A complete fifth-nerve lesion on one side causes unilateral sensory loss on the face, tongue and buccal mucosa. The jaw deviates to the side of the lesion when the mouth is opened. A brisk jaw jerk is seen with upper motor neurone lesions, i.e. above the motor nucleus in the pons.

Fig. 17.8 Cutaneous distribution of the trigeminal nerve. (1) ophthalmic or first division; (2), maxillary or second division; (3), mandibular or third division.

A fifth nerve lesion is due to pathology within the brainstem (tumour, multiple sclerosis, infarction, syringobulbia), at the cerebellopontine angle (acoustic neuroma, other tumour), within the petrous temporal bone (spread-ing middle ear infection) or within the cavernous sinus (aneurysm of the internal carotid artery, tumour, thrombosis of the cavernous sinus).

Trigeminal neuralgia

Trigeminal neuralgia (tic douloureux) is of unknown cause, seen most com-monly in old age, and is almost always unilateral.

Clinical features

Severe paroxysms of knife-like pain occur in one or more sensory divisions of the trigeminal nerve (see above), although rarely in the ophthalmic division. Each paroxysm is stereotyped, brought on by stimulation of a specific ‘trigger zone’ in the face. The stimuli may be minimal, and include washing, shaving and eating. There are no objective physical signs and the diagnosis is based on the history.

Management

The anticonvulsant carbamazepine suppresses attacks in most patients. Phenytoin and gabapentin are also used but are less effective. If this fails, thermocoagulation of the trigeminal ganglion or section of the sensory division may be necessary.

Differential diagnosis

Similar pain may occur with structural lesions involving the trigeminal nerve. These lesions are often accompanied by physical signs, e.g. a depressed corneal reflex.

The facial nerve (seventh cranial nerve)

The facial nerve is largely motor in function, supplying the muscles of facial expression. It has, in addition, two major branches: the chorda tympani, which carries taste from the anterior two-thirds of the tongue, and the nerve to the stapedius muscle (this has a damping effect to protect the ear from loud noise). These two branches arise from the facial nerve during its intra-cranial course through the facial canal of the petrous temporal bone. There-fore, damage to the facial nerve in the temporal bone (e.g. Bell's palsy, trauma, herpes zoster, middle-ear infection) may be associated with undue sensitivity to sounds (hyperacusis) and loss of taste to the anterior two-thirds of the tongue.

Lower motor neurone (LMN) lesions

A unilateral LMN lesion causes weakness of all the muscles of facial expres-sion (cf. UMN, see below) on the same side as the lesion. The face, especially the angle of the mouth, falls and dribbling occurs from the corner of the mouth. There is weakness of frontalis, the eye will not close and the exposed cornea is at risk of ulceration. LMN facial palsy is caused by a lesion in the pons/medulla (and involving the VII cranial nerve nuclei) or a by a lesion in the course of the facial nerve outside of the brainstem (posterior fossa, facial canal in the temporal bone, middle ear, parotid gland). The nerve may also be affected in polyneuritis (e.g. Guillain-Barré syndrome, Lyme disease), when there may be bilateral involvement. The commonest cause of LMN facial palsy is Bell's palsy.

Bell’s palsy This is a common, acute, isolated unilateral facial nerve palsy that is probably the result of a viral infection (often herpes simplex) that causes swelling of the nerve within the petrous temporal bone. Peak inci-dence is between the ages of 65 and 74 years and it is more common in pregnancy.

Clinical features

There is LMN weakness of the facial muscles, sometimes with loss of taste on the anterior two-thirds of the tongue. There may be hyperacusis and decreased production of tears.

Investigations

The diagnosis is clinical. The differential diagnosis of LMN facial weakness includes the Ramsay Hunt syndrome (see below) and parotid gland tumour. In addition, the facial nerve is the commonest cranial nerve lesion in meningitis associated with Lyme disease (erythema migrans on the limbs and trunk in a patient with a history of tick bite, p. 21) and in sarcoidosis (p. 547), in which bilateral involvement may occur. Bilateral Bell's palsy is rare. A prolonged steadily progressive weakness suggests a tumour.

Management

The eyelid must be closed to protect the cornea from ulceration (either adhesive tape or, in prolonged cases surgical tarsorraphy). Oral prednisolone (60 mg/day for 10 days) given within 72 hours of onset increases the chance of a full recovery. Antivirals (e.g. valaciclovir) are used in addition in severe cases.

Prognosis

Most patients recover completely, although 30% are left with a permanent weakness.

Ramsay Hunt syndrome This is herpes zoster (shingles) of the genicu-late ganglion (the sensory ganglion for taste fibres) situated in the facial canal. There is an LMN facial palsy, with herpetic vesicles in the external auditory meatus and sometimes in the soft palate. Deafness may occur as a result of involvement of the eighth nerve in the facial canal. Treatment is with aciclovir.

Upper motor neurone (UMN) lesions

An upper motor neurone lesion causes weakness of the lower part of the face on the side opposite the lesion. Upper facial muscles are spared because of the bilateral cortical innervation of neurones supplying the upper face. Wrinkling of the forehead (frontalis muscle) and eye closure are normal. The most common cause is a stroke, when there is an associated hemiparesis.

The vestibulocochlear nerve (eighth cranial nerve)

The eighth cranial nerve has two components: cochlear and vestibular, sub-serving hearing and equilibrium respectively (Fig. 16.1). The clinical features of a cochlear nerve lesion are sensorineural deafness and tinnitus. Causes of a cochlear nerve lesion are within the brainstem (tumour, multiple sclero-sis, infarction), cerebellopontine angle (acoustic neuroma and other tumours) and petrous temporal bone (trauma, middle ear infection, tumour). Sensori-neural deafness may also be the result of disease of the cochlea itself: Ménière's disease (p. 705), drugs (e.g. gentamicin) and presbyacusis (deaf-ness of old age).

The main symptom of a vestibular nerve lesion is vertigo, which may be accompanied by vomiting. Nystagmus is the principal physical sign, often with ataxia (loss of balance).

Vertigo

Vertigo is the definite illusion of movement - a sensation as if the external world were revolving around the patient. It results from disease of the inner ear, the eighth nerve or its central connections (p. 704).

Nystagmus

Nystagmus is a rhythmic oscillation of the eyes, which must be sustained for more than a few beats to be significant. It is a sign of disease of either the ocular or the vestibular system and its connections. Nystagmus is described as either pendular or jerk.

Pendular nystagmus A pendular movement of the eye occurs; there is no rapid phase. It occurs where there is poor visual fixation (i.e. long-standing severe visual impairment) or a congenital lesion.

Jerk nystagmus Jerk nystagmus has a fast and a slow component to the rhythmic movement:

■ Horizontal or rotary nystagmus may be either peripheral (middle ear) or central (brainstem and cerebellum) in origin. In peripheral lesions it is usually transient (minutes or hours); in central lesions it is long lasting (weeks, months or more).

■ Vertical nystagmus is caused only by central lesions.

Glossopharyngeal, vagus, accessory and hypoglossal nerves (ninth to twelfth cranial nerves)

The lower four cranial nerves (ninth to twelfth) which lie in the medulla (the ‘bulb’) are usually affected together; isolated lesions are rare. A bulbar palsy is a weakness of the lower motor neurone type, of the muscles supplied by these cranial nerves. There is dysarthria, dysphagia and nasal regurgitation. The tongue is weak, wasted and fasciculating The most common causes of a bulbar palsy are motor neurone disease (p. 782), syringobulbia (p. 780) and Guillain-Barré syndrome (p. 788). Poliomyelitis is now rare. Pseudobulbar palsy is an upper motor neurone weakness of the same muscle groups. There is also dysarthria, dysphagia and nasal regurgitation, but the tongue is small and spastic and there is no fasciculation. The jaw jerk is exaggerated and the patient is emotionally labile. In many patients there is a partial palsy with only some of these features. The most common cause of pseudobulbar palsy is a stroke, but it may also occur in motor neurone disease and multiple sclerosis.

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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