Learn — Nervous system & special senses

18 notes · 43 questions on the topic

Upper limb — nerve supply

The upper limb is supplied by the brachial plexus, formed from the ventral rami of C5 to T1, which reorganises through roots, trunks, divisions, cords and branches into five terminal nerves — musculocutaneous, axillary, radial, median and ulnar. Each nerve has a signature motor loss and a signature patch of sensory loss, and it is those matched pairs that let a nurse place the level of an injury at the bedside and that the examiner asks for.

The plan of the plexus is roots C5 to T1, upper (C5 and C6), middle (C7) and lower (C8 and T1) trunks, anterior and posterior divisions, then lateral, posterior and medial cords named for their position around the axillary artery, and finally the five terminal branches.
Axillary nerve (C5, C6) supplies deltoid and teres minor and the regimental-badge patch of skin over the deltoid; it winds round the surgical neck of the humerus, so a fracture there or an anterior shoulder dislocation loses abduction beyond the first 15 degrees and sensation over that patch.
Musculocutaneous nerve (C5, C6, C7) supplies coracobrachialis, biceps brachii and brachialis — elbow flexion and powerful supination — and continues as the lateral cutaneous nerve of the forearm; the biceps jerk tests C5 and C6.
Radial nerve (C5 to T1, from the posterior cord) supplies every extensor of the elbow, wrist and fingers along with brachioradialis and supinator; it lies in the spiral groove of the humerus, so a mid-shaft humeral fracture, a crutch pressed into the axilla or an arm hung over a chair back gives wrist drop with sensory loss over the first dorsal web space, and the triceps jerk tests C7.
Median nerve (C6 to T1) supplies most forearm flexors and the thenar muscles remembered as LOAF — the lateral two lumbricals, opponens pollicis, abductor pollicis brevis and flexor pollicis brevis — with sensation over the lateral three and a half digits on the palm; injury at the wrist wastes the thenar eminence and abolishes opposition (ape hand), and a high injury adds the hand of benediction on trying to make a fist.
Ulnar nerve (C8, T1) supplies flexor carpi ulnaris, the medial half of flexor digitorum profundus and all the small muscles of the hand except LOAF, with sensation over the medial one and a half digits; it lies behind the medial epicondyle, and injury gives claw hand, wasting of the first dorsal interosseous and a positive Froment's sign.
Erb's palsy is an upper trunk (C5, C6) injury from traction on the shoulder at birth or a fall on the shoulder: the arm hangs adducted, medially rotated and pronated in the waiter's-tip position. Klumpke's palsy is a lower trunk (C8, T1) injury giving a claw hand, and it may add Horner's syndrome because the T1 root carries sympathetic fibres.
The safe deltoid intramuscular injection site is in the thickest part of the muscle, 2.5 to 5 cm (two to three finger-breadths) below the acromion process, with a maximum volume of about 1 mL in an adult; injecting lower or more posteriorly risks the axillary nerve as it winds round the humerus and the radial nerve further down the arm.
In the antecubital fossa, remember the order from lateral to medial for cannulation and venepuncture — the brachial artery and the median nerve lie medial to the biceps tendon, so a cannula sited too medially and too deep can strike both.

CSF — production and volume

Cerebrospinal fluid is the clear, colourless fluid that fills the ventricles and the subarachnoid space and lets the 1,400 g brain float with an effective weight of only about 50 g, cushioning it and carrying away metabolites. It is secreted continuously by the choroid plexuses and absorbed continuously into the venous sinuses, so its volume, pressure and composition are tightly held, and any block in that circuit raises the intracranial pressure.

Total volume in an adult is about 150 mL, of which roughly 25 mL is in the ventricles; about 500 mL is formed each day, so the whole volume is replaced three to four times in 24 hours.
Production is by the choroid plexuses of the lateral, third and fourth ventricles at about 0.35 mL a minute (roughly 20 mL an hour), and it is an active secretion that continues largely regardless of the intracranial pressure — which is why a block causes hydrocephalus rather than simply stopping the flow.
The path runs from the lateral ventricles through the interventricular foramina of Monro to the third ventricle, through the cerebral aqueduct of Sylvius to the fourth ventricle, then out through the two lateral foramina of Luschka and the median foramen of Magendie into the subarachnoid space and the central canal.
Absorption is by bulk flow through the arachnoid villi and granulations into the superior sagittal sinus, through one-way valves that open once the CSF pressure exceeds the venous sinus pressure.
Normal lumbar opening pressure in the lateral position is 6 to 18 cm of water, and the normal intracranial pressure is 5 to 15 mmHg.
Normal composition: crystal clear, 0 to 5 lymphocytes per cubic millimetre, protein 15 to 45 mg/dL, glucose 45 to 80 mg/dL (about two thirds of the simultaneous blood glucose) and chloride higher than plasma at about 118 to 132 mEq/L.
The classic patterns: bacterial meningitis gives turbid fluid with hundreds to thousands of neutrophils, high protein and low glucose; viral meningitis gives clear fluid with lymphocytes, mildly raised protein and normal glucose; tuberculous meningitis gives lymphocytes, a very high protein, a low glucose and a cobweb clot on standing.
In the adult the spinal cord ends at the lower border of L1, so a lumbar puncture is done at the L3 to L4 or L4 to L5 space, located by the line joining the highest points of the iliac crests; in an infant the cord reaches about L3, so the puncture is made at L4 to L5 or lower.
Communicating hydrocephalus is a failure of absorption after meningitis or subarachnoid haemorrhage, while non-communicating or obstructive hydrocephalus is a block within the ventricular system, most often at the narrow cerebral aqueduct.

Parasympathetic nervous system

The parasympathetic division is the craniosacral outflow of the autonomic nervous system, the rest, digest and repair half that conserves energy and empties hollow organs. Its preganglionic fibres are long and end in ganglia on or within the target organ, so its effects are discrete and organ by organ rather than the mass discharge of the sympathetic system.

The outflow is craniosacral: cranial nerves III, VII, IX and X, and the sacral segments S2, S3 and S4 through the pelvic splanchnic nerves (nervi erigentes).
The vagus alone carries about 75 per cent of all parasympathetic fibres and supplies the heart, lungs and gut as far as the junction of the proximal two thirds with the distal third of the transverse colon; the rest of the colon and the pelvic organs are supplied from S2 to S4.
Acetylcholine is the transmitter at both synapses: preganglionic fibres act on nicotinic receptors in the ganglion and postganglionic fibres on muscarinic receptors at the effector, so a muscarinic blocker such as atropine abolishes the effects while leaving the ganglion working.
The four cranial parasympathetic ganglia and their nerves are the ciliary (III), the pterygopalatine and submandibular (VII) and the otic (IX).
Effects: constriction of the pupil by the sphincter pupillae and accommodation, watery salivation and lacrimation, slowing of the sinoatrial node, bronchoconstriction with increased mucus, increased gut motility and secretion with sphincter relaxation, detrusor contraction with internal sphincter relaxation, and penile erection.
There is no parasympathetic supply to sweat glands, arrector pili muscles, the adrenal medulla or most blood vessels — these are sympathetic only, which is why atropine leaves a patient dry, flushed and hot.
Muscarinic subtypes: M2 slows the heart, M3 contracts smooth muscle and drives glandular secretion, and M1 acts in the stomach and central nervous system.
Vagal stimulation from deep suctioning, nasogastric tube insertion, straining at stool, carotid sinus pressure or a distended bladder can drop the heart rate abruptly; atropine 0.5 to 1 mg intravenously, repeated as ordered, reverses symptomatic vagal bradycardia.

Nerve physiology

A neurone carries information as a self-propagating change in membrane voltage, the action potential, generated by the sequential opening of voltage-gated sodium and potassium channels across a membrane that the sodium-potassium pump keeps polarised. Every drug that numbs, every electrolyte disturbance that weakens and every demyelinating disease that slows a patient acts somewhere in this sequence, which is why it is examined so heavily.

The resting membrane potential of a neurone is about -70 mV, and about -90 mV in skeletal and cardiac muscle; it is set mainly by the leak of potassium out of the cell down its concentration gradient.
The sodium-potassium ATPase pumps 3 sodium ions out for every 2 potassium ions in, so it is electrogenic and contributes a few millivolts of the resting negativity as well as maintaining the gradients each action potential spends.
A stimulus that depolarises the membrane to a threshold of about -55 mV opens voltage-gated sodium channels, sodium rushes in and the potential overshoots to about +35 mV.
Repolarisation follows as the sodium channels inactivate and slower voltage-gated potassium channels open; the continued potassium efflux produces a brief after-hyperpolarisation below the resting level.
During the absolute refractory period the sodium channels are inactivated and no stimulus of any strength can fire the cell; during the relative refractory period a stronger than normal stimulus can. This sets the maximum firing frequency and makes the impulse travel in one direction only.
The action potential obeys the all-or-none law: once threshold is reached the size of the spike is fixed, and stimulus strength is coded as the frequency of firing and the number of fibres recruited, never as a bigger spike.
Myelin, from Schwann cells in the peripheral nervous system and oligodendrocytes in the central nervous system, insulates the axon so that current jumps from one node of Ranvier to the next — saltatory conduction, which is both faster and far cheaper in energy.
Conduction velocity rises with fibre diameter and myelination: large myelinated A-alpha fibres conduct at about 70 to 120 metres per second, while unmyelinated C fibres carrying slow burning pain conduct at about 0.5 to 2 metres per second.
Local anaesthetics such as lignocaine block the voltage-gated sodium channel and abolish the action potential; small unmyelinated pain fibres are blocked before large motor fibres, which is why sensation is lost before power.

Brain physiological functions

The brain weighs about 1,400 g, some 2 per cent of body weight, yet it takes about 15 per cent of the cardiac output and 20 per cent of the body's oxygen, and it holds no store of glucose or oxygen of its own. Its functions are localised — each lobe, the cerebellum, the basal ganglia, the diencephalon and the brainstem do distinct work — so the deficit at the bedside tells the nurse where the lesion is.

Frontal lobe: the precentral gyrus (Brodmann area 4) is the primary motor cortex carrying the motor homunculus, while the prefrontal cortex holds personality, judgement, planning and social restraint; Broca's area (areas 44 and 45) lies in the inferior frontal gyrus of the dominant hemisphere.
Parietal lobe: the postcentral gyrus (areas 3, 1 and 2) is the primary somatosensory cortex; the non-dominant parietal lobe carries spatial awareness, and its lesion causes neglect of the opposite side, so the patient bumps into doorframes and eats only half the plate.
Temporal lobe: the primary auditory cortex (areas 41 and 42), Wernicke's area (area 22) in the dominant hemisphere, the hippocampus for laying down new memory and the amygdala for emotion.
Occipital lobe: the primary visual cortex (area 17) around the calcarine sulcus, with the macula represented at the occipital pole, which has a dual blood supply and is often spared in a posterior cerebral artery stroke.
Cerebellum: coordination, balance, muscle tone and the timing of movement, with signs on the same side as the lesion — ataxia, intention tremor, nystagmus, dysdiadochokinesia and a broad-based gait.
The thalamus relays every sensation except smell to the cortex, the hypothalamus controls temperature, hunger, thirst, the autonomic system and the pituitary, and the basal ganglia set the initiation and smoothness of movement, their failure giving the rigidity and tremor of Parkinson's disease.
Brainstem: the midbrain carries pupillary and postural reflexes, the pons holds the pneumotaxic and apneustic respiratory centres, and the medulla holds the vital vasomotor, cardiac and respiratory centres, so a medullary lesion is fatal; the reticular activating system maintains consciousness.
Cerebral blood flow is about 50 to 55 mL per 100 g of brain per minute and is autoregulated over a mean arterial pressure of roughly 60 to 150 mmHg; cerebral perfusion pressure is the mean arterial pressure minus the intracranial pressure and is kept above about 60 mmHg.
Carbon dioxide is the most powerful cerebral vasodilator, so a rising PaCO2 increases cerebral blood flow and intracranial pressure — the reason the airway and ventilation come before everything else in a head injury.

Broca vs Wernicke area

Broca's and Wernicke's areas are the two language centres of the dominant hemisphere, which is the left in about 95 per cent of right-handed people and in most left-handed people as well. Broca's area in the inferior frontal gyrus produces speech, Wernicke's area in the posterior superior temporal gyrus understands it, and the arcuate fasciculus joins the two — so which one is damaged decides whether the patient cannot speak or cannot make sense.

Broca's area is the pars opercularis and pars triangularis of the inferior frontal gyrus (Brodmann areas 44 and 45), supplied by the superior division of the middle cerebral artery.
Broca's expressive, motor or non-fluent aphasia: speech is sparse, effortful and telegraphic with poor grammar and repetition is impaired, but comprehension is preserved, so the patient follows commands and is painfully aware of the failure and frustrated by it.
Because the motor cortex lies next door, Broca's aphasia usually comes with a right-sided weakness affecting the face and arm more than the leg.
Wernicke's area is the posterior part of the superior temporal gyrus (Brodmann area 22), supplied by the inferior division of the middle cerebral artery.
Wernicke's receptive, sensory or fluent aphasia: speech flows freely with normal rhythm but is full of wrong and invented words, comprehension is lost, repetition is impaired and the patient is typically unaware of the problem — which is easily mistaken for confusion or a psychiatric illness.
A right superior quadrantanopia may accompany Wernicke's aphasia because the temporal fibres of the optic radiation (Meyer's loop) run beneath the area, while limb power is usually normal — which is why this stroke is so often missed.
The arcuate fasciculus connects the two areas, and its lesion gives conduction aphasia: fluent speech with intact comprehension but disproportionately poor repetition.
Global aphasia, with both production and comprehension lost, follows occlusion of the middle cerebral artery trunk; in the transcortical aphasias a watershed lesion spares repetition, so the patient can repeat what is said without being able to use it.
Aphasia is a disorder of language, not of speech: dysarthria is weak articulation with normal language and dysphonia is a disorder of voice, and the distinction changes both the site of the lesion and the therapy.

Sympathetic nervous system

The sympathetic division is the thoracolumbar outflow of the autonomic nervous system, arising from the lateral horn of the spinal cord between T1 and L2. Its short preganglionic fibres reach the paravertebral sympathetic chain where each synapses with many long postganglionic fibres, so the system discharges as a mass and prepares the whole body at once for fight or flight.

The outflow is thoracolumbar, T1 to L2, from the intermediolateral cell column; the fibres leave in the ventral roots as white rami communicantes and rejoin the spinal nerves as grey rami.
Preganglionic fibres are short and release acetylcholine onto nicotinic receptors in the ganglion, while postganglionic fibres are long and release noradrenaline — except at the sweat glands, where the postganglionic sympathetic fibres are cholinergic and act on muscarinic receptors.
The adrenal medulla is a modified sympathetic ganglion supplied directly by preganglionic fibres; its chromaffin cells release about 80 per cent adrenaline and 20 per cent noradrenaline straight into the blood, prolonging the response.
Receptor map: alpha-1 constricts vessels, dilates the pupil through the radial muscle and contracts the bladder neck; alpha-2 is presynaptic and inhibits further noradrenaline release; beta-1 raises heart rate, contractility and renin; beta-2 dilates bronchi and skeletal muscle vessels and relaxes the uterus; beta-3 acts on fat and the detrusor.
Effects: the pupils dilate, the mouth goes dry, the heart races and contracts harder, the bronchi open, the gut and bladder shut down, the skin becomes pale and sweaty, glycogen and fat are mobilised and blood is diverted to skeletal muscle.
The cardiac accelerator fibres arise from T1 to T5 — the same segments that carry cardiac pain, which is why angina is felt in the chest, the left arm and the jaw.
The sympathetic supply to the head travels up from T1 through the cervical chain to the superior cervical ganglion, and interruption anywhere along that path gives Horner's syndrome: partial ptosis, a constricted pupil, anhidrosis of the face and an apparently sunken eye.
Only the sympathetic system supplies sweat glands, arrector pili muscles, the adrenal medulla and most blood vessels, so vasomotor tone and thermoregulatory sweating are lost below a cord lesion — giving the warm, dry, pink skin of neurogenic shock.

Root values of reflexes (knee jerk L3-L4)

A deep tendon reflex is a monosynaptic stretch reflex: the tendon tap stretches the muscle spindle, the Ia afferent fires into the cord and, across a single synapse, the alpha motor neurone of the same muscle contracts. Because each reflex is wired to one or two named spinal segments, the presence, absence or exaggeration of a reflex localises a lesion far more reliably than a patient's description of weakness.

Knee jerk (patellar, quadriceps, femoral nerve): L2, L3 and L4 — quoted in examinations as L3 and L4.
Ankle jerk (Achilles, gastrocnemius and soleus, tibial nerve): S1 and S2.
Biceps jerk: C5 and C6 through the musculocutaneous nerve; supinator or brachioradialis jerk: C5 and C6 through the radial nerve.
Triceps jerk: C6, C7 and C8, mainly C7, through the radial nerve.
Superficial reflexes: the plantar response is L5, S1 and S2; the cremasteric reflex is L1 and L2; the abdominal reflexes are T7 to T9 above the umbilicus and T10 to T12 below it; the anal reflex is S4 and S5.
Cranial reflex arcs: the corneal reflex has an ophthalmic trigeminal (V1) afferent and a facial (VII) efferent, the gag reflex a glossopharyngeal (IX) afferent and a vagal (X) efferent, and the pupillary light reflex an optic (II) afferent and an oculomotor (III) efferent.
Reflexes are graded 0 to 4: 0 absent, 1+ diminished, 2+ normal, 3+ brisk and possibly still normal, and 4+ exaggerated with clonus.
An absent or reduced reflex points to the lower motor neurone or the arc itself — a root lesion, a peripheral neuropathy, a muscle disease or spinal shock — while an exaggerated reflex with clonus and an extensor plantar points to an upper motor neurone lesion above that segment.
The Jendrassik manoeuvre, asking the patient to interlock the fingers and pull while the lower limb reflex is tested, reinforces a reflex that seems absent and should be used before recording one as lost.
Counted from the ground upwards the pairs run in order: ankle S1 and S2, knee L3 and L4, biceps and supinator C5 and C6, triceps C7 and C8.

Brachial and cervical plexus

The cervical plexus (C1 to C4) and the brachial plexus (C5 to T1) are the two networks formed by the anterior rami of the cervical nerves; the first supplies the skin of the neck, the strap muscles and the diaphragm, and the second supplies the whole upper limb. Because both lie superficially in the neck and axilla they are injured by traction at birth, by fractures and by careless positioning, and each pattern of loss is recognisable at the bedside.

The cervical plexus is formed by the anterior rami of C1 to C4 and lies deep to the sternocleidomastoid; its cutaneous branches are the lesser occipital (C2), great auricular (C2 and C3), transverse cervical (C2 and C3) and supraclavicular (C3 and C4) nerves.
All four cutaneous branches emerge at the nerve point of the neck, or Erb's point, at the middle of the posterior border of the sternocleidomastoid — the landmark for a superficial cervical plexus block.
The phrenic nerve arises from C3, C4 and C5 with its main root from C4 and is the only motor supply to the diaphragm; the ansa cervicalis, from C1 to C3, supplies the infrahyoid strap muscles.
The brachial plexus is formed by the anterior rami of C5 to T1 and runs roots, trunks, divisions, cords and branches; the roots and trunks lie in the posterior triangle, the divisions behind the clavicle and the cords and branches in the axilla.
The trunks are upper (C5 and C6), middle (C7) and lower (C8 and T1); the three cords are named lateral, posterior and medial from their relation to the second part of the axillary artery.
The five terminal branches are the musculocutaneous (C5 to C7, lateral cord), axillary (C5 and C6, posterior cord), radial (C5 to T1, posterior cord), median (C6 to T1, from the lateral and medial cords) and ulnar (C8 and T1, medial cord).
Erb-Duchenne palsy is an upper trunk (C5 and C6) injury from downward traction on the shoulder, as in shoulder dystocia or a fall on the shoulder, giving the waiter's tip position — arm adducted and internally rotated, elbow extended, forearm pronated — with sensory loss over the deltoid.
Klumpke's palsy is a lower trunk (C8 and T1) injury from traction on an abducted arm, giving a claw hand with wasted small muscles, and Horner's syndrome when the T1 sympathetic fibres are torn.
Nerves at risk with fractures: the axillary nerve with a surgical neck of humerus fracture, causing deltoid paralysis and loss of sensation over the regimental badge area, the radial nerve in the spiral groove with a mid-shaft humeral fracture, causing wrist drop, and the ulnar nerve behind the medial epicondyle.

Thermoregulatory centre (hypothalamus)

The hypothalamus is the body's thermostat: the preoptic and anterior hypothalamic nuclei sense the temperature of the blood flowing through them and of the skin, compare it with a set point of about 37 degrees Celsius, and drive heat loss or heat gain until the two match. Fever is not a failure of that thermostat but a deliberate resetting of it upwards by pyrogens, which is why a febrile patient shivers while the temperature is climbing.

The anterior and preoptic hypothalamus is the heat loss centre, producing cutaneous vasodilatation, sweating and inhibition of heat production; its destruction causes hyperthermia.
The posterior hypothalamus is the heat gain and conservation centre, producing cutaneous vasoconstriction, shivering and piloerection; its destruction causes hypothermia.
Normal core temperature is 36.5 to 37.5 degrees Celsius with a diurnal swing of about 0.5 to 1 degree, lowest in the early morning and highest in the late afternoon; the rectal reading is about 0.5 degrees above the oral and the axillary about 0.5 degrees below it.
Heat is lost by radiation, conduction, convection and evaporation, including an insensible loss of some 600 to 800 mL a day from skin and lungs; once the ambient temperature exceeds body temperature, evaporation is the only route left.
Shivering can raise heat production to four or five times the basal rate; the shivering centre lies in the posterior hypothalamus and is normally held in check by the anterior hypothalamus.
In fever, exogenous pyrogens such as bacterial lipopolysaccharide make macrophages release the endogenous pyrogens interleukin-1, interleukin-6, tumour necrosis factor and the interferons, which raise prostaglandin E2 in the anterior hypothalamus and lift the set point.
While the set point is rising the patient feels cold, shivers and has rigors with vasoconstriction; when it falls again, by crisis or by lysis, the patient flushes and sweats. Antipyretics work by inhibiting cyclo-oxygenase and lowering the set point.
Hyperthermia is not fever: in heat stroke, malignant hyperthermia and neuroleptic malignant syndrome the set point is normal and the heat-losing mechanisms are overwhelmed or blocked, so the treatment is active physical cooling, with dantrolene in malignant hyperthermia, and antipyretics do not work.
Newborns cannot shiver and generate heat by metabolising brown adipose tissue (non-shivering thermogenesis); they lose heat fast through a large surface area to weight ratio and thin skin, which is why the delivery room is kept warm and the baby is dried and wrapped immediately.

Cervical nerves

There are eight pairs of cervical spinal nerves but only seven cervical vertebrae, so the numbering shifts at the base of the neck: the first seven emerge above the vertebra of the same number and the eighth emerges between the seventh cervical and the first thoracic vertebra. Below that, every spinal nerve leaves below the vertebra of its own number, and this one-level shift is what makes localisation of a cervical lesion an examination favourite.

There are 31 pairs of spinal nerves in all: 8 cervical, 12 thoracic, 5 lumbar, 5 sacral and 1 coccygeal.
C1 to C7 exit through the intervertebral foramen above the corresponding vertebra, C8 exits between C7 and T1, and from T1 downwards each nerve exits below its own vertebra.
The first cervical nerve, the suboccipital nerve, is essentially motor and usually has no cutaneous territory; the anterior rami of C1 to C4 form the cervical plexus and those of C5 to T1 form the brachial plexus.
Key dermatomes: C2 the back of the scalp, C3 the neck, C4 the clavicle and point of the shoulder, C5 the lateral arm over the deltoid, C6 the thumb, C7 the middle finger, C8 the little finger and T1 the medial forearm.
Key myotomes: C5 shoulder abduction and elbow flexion, C6 wrist extension, C7 elbow extension, C8 finger flexion and T1 finger abduction — the sequence tested to record a motor level.
The phrenic nerve carries C3, C4 and C5 and is the only motor supply to the diaphragm; irritation of the diaphragm by blood, air or an inflamed gallbladder beneath it is felt at the tip of the shoulder, because the C4 dermatome covers that skin.
A cervical disc prolapse compresses the root numbered below the disc, so a C5 to C6 disc irritates the C6 root and gives pain and numbness into the thumb with a reduced biceps jerk.
The vertebral level and the cord segment do not correspond, because the cord is shorter than the canal; in the cervical region the cord segment lies about one level above the vertebral spine of the same number.

Cranial nerves — 12

The twelve pairs of cranial nerves arise from the brain and brainstem and leave the skull through named foramina to supply the head and neck, with the vagus reaching as far as the transverse colon. Each has a fixed number, a fixed function and a fixed exit, and cranial nerve testing is the fastest bedside way to localise a brainstem lesion, a raised intracranial pressure or a stroke.

The twelve in order: I olfactory, II optic, III oculomotor, IV trochlear, V trigeminal, VI abducens, VII facial, VIII vestibulocochlear, IX glossopharyngeal, X vagus, XI accessory, XII hypoglossal.
Purely sensory: I, II and VIII. Purely motor: III, IV, VI, XI and XII. Mixed: V, VII, IX and X.
Attachments: I and II are outgrowths of the forebrain, III and IV arise from the midbrain, V, VI, VII and VIII from the pons and the pontomedullary junction, and IX, X, XI and XII from the medulla.
The trochlear (IV) is the only cranial nerve to leave from the back of the brainstem and the only one to decussate completely, so it has the longest intracranial course and is easily damaged in head injury.
Exits: I through the cribriform plate, II through the optic canal, III, IV, V1 and VI through the superior orbital fissure, V2 through the foramen rotundum, V3 through the foramen ovale, VII and VIII through the internal acoustic meatus with VII leaving the skull at the stylomastoid foramen, IX, X and XI through the jugular foramen, and XII through the hypoglossal canal.
Four cranial nerves carry parasympathetic fibres: III to the ciliary ganglion for pupil constriction and accommodation, VII to the pterygopalatine and submandibular ganglia for tears and saliva, IX to the otic ganglion for the parotid, and X to the thoracic and abdominal viscera.
Reflex pairs: the pupillary light reflex is II in and III out, the corneal reflex V1 in and VII out, the gag reflex IX in and X out, and the jaw jerk V in and V out.
The trigeminal is the largest cranial nerve, the chief sensory nerve of the face with motor supply to the muscles of mastication; the vagus is the longest, and its recurrent laryngeal branch supplies the vocal cords.
A lower motor neurone facial (VII) palsy such as Bell's palsy weakens the whole half of the face including the forehead and leaves the eye unable to close, while an upper motor neurone lesion from a stroke spares the forehead because the upper face has bilateral cortical supply.

Plantar reflex

The plantar reflex is a superficial cutaneous reflex with the root value L5, S1 and S2, elicited by stroking the sole with a blunt point along the lateral border from the heel forward and then medially across the ball of the foot. The normal adult answer is flexion of the great toe, and an extensor answer — the Babinski sign — means the corticospinal tract that normally suppresses it has been damaged, making it one of the few signs in medicine that cannot be faked.

The root value is L5, S1 and S2, with the afferent and efferent limbs travelling in the tibial branch of the sciatic nerve; unlike a knee jerk it is polysynaptic and superficial, so it is lost in deep sleep, anaesthesia and coma.
Technique: use a blunt object such as an orange stick or a key and never a pin, stroke firmly and slowly up the lateral border of the sole and curve medially across the metatarsal heads, and watch the first movement of the great toe.
The normal flexor response is plantar flexion of the great toe with flexion of the other toes; the abnormal extensor or Babinski response is dorsiflexion of the great toe with fanning of the other toes.
An extensor plantar in an adult indicates an upper motor neurone lesion anywhere in the corticospinal tract — stroke, cord compression, multiple sclerosis, motor neurone disease or a space-occupying lesion — and usually goes with spasticity, brisk reflexes and clonus.
The extensor response is normal until about 1 to 2 years of age because the corticospinal tract is not yet myelinated; persistence beyond about 2 years is abnormal.
Equivalents used when the sole is ticklish, dressed or anaesthetic: Chaddock's sign by stroking below the lateral malleolus, Oppenheim's sign by running the knuckles down the shin, Gordon's sign by squeezing the calf and Schaefer's sign by squeezing the Achilles tendon.
A transient extensor plantar occurs after a generalised seizure with Todd's paresis, in deep coma, in hypoglycaemia and under general anaesthesia, so it must be interpreted with the rest of the examination.
The plantar response is absent, neither flexor nor extensor, when the arc itself is broken as in a peripheral neuropathy or a sole that has lost sensation, and this must be recorded as absent rather than as normal.

Eye — parts and vision

The eyeball is built from three concentric coats, an outer fibrous coat of cornea and sclera, a middle vascular coat or uvea made of iris, ciliary body and choroid, and an inner nervous coat, the retina, with the aqueous humour, lens and vitreous filling it as its refractive media. Light is bent by the cornea and the lens onto the retina, where rods and cones convert it into nerve impulses that travel by the optic nerve to the occipital cortex, so a nurse who knows this map can tell a painful red eye from a painless loss of vision at the bedside.

Outer fibrous coat: the transparent avascular cornea in front, nourished by tears and aqueous humour and richly supplied with sensory endings from the ophthalmic division of the trigeminal nerve, continuous with the opaque white sclera behind at the limbus.
Middle vascular coat: the iris with its central pupil, the ciliary body containing the ciliary muscle of accommodation and the epithelium that secretes aqueous humour, and the choroid, which supplies the outer retina.
The cornea is the strongest refracting surface of the eye and provides roughly two-thirds of the total refractive power of about 60 dioptres; the lens supplies the rest and is the only adjustable part, changing shape for accommodation.
Aqueous humour is secreted by the ciliary epithelium into the posterior chamber, flows through the pupil into the anterior chamber and drains at the angle through the trabecular meshwork into the canal of Schlemm; obstruction raises intraocular pressure above the normal 10 to 21 mmHg and causes glaucoma.
The retina holds about 120 million rods, which contain rhodopsin, lie peripherally and give black-and-white vision in dim light, and about 6 to 7 million cones, which are concentrated at the macula and give colour and fine detail in bright light through three pigments sensitive to red, green and blue.
The fovea centralis at the centre of the macula contains only cones and is the point of maximum visual acuity, while the optic disc where the nerve leaves has no photoreceptors at all and is the physiological blind spot.
Accommodation for near vision is parasympathetic through the oculomotor nerve and the ciliary ganglion: the ciliary muscle contracts, the suspensory zonules slacken and the lens becomes more convex, together with pupillary constriction and convergence.
Refractive errors: in myopia the image falls in front of the retina and is corrected with a concave (minus) lens; in hypermetropia it falls behind and is corrected with a convex (plus) lens; astigmatism needs a cylindrical lens; and presbyopia is the loss of lens elasticity after about 40 years that requires a reading addition.
The visual pathway runs retina, optic nerve, optic chiasma where the nasal fibres cross, optic tract, lateral geniculate body of the thalamus, optic radiation and primary visual cortex around the calcarine sulcus of the occipital lobe, so a lesion at the chiasma gives bitemporal hemianopia and one behind it gives a homonymous field loss.
Vitamin A deficiency damages rod function first and produces night blindness, then Bitot's spots and xerophthalmia, and it remains a preventable cause of childhood blindness in India.

Agnosia

Agnosia is the loss of the ability to recognise or interpret sensory information even though the sense organ, the primary sensory cortex, attention, language and general intelligence are all intact. The failure is in the association cortex, where raw sensation is given meaning, so the patient sees the object perfectly but cannot say what it is, which separates agnosia from blindness, from aphasia and from apraxia.

Visual agnosia is the failure to recognise objects by sight with normal acuity and normal visual fields, and it follows lesions of the occipitotemporal association cortex; the patient can identify the same object at once by touch or by sound.
Prosopagnosia is the specific inability to recognise familiar faces, including sometimes the patient's own, and it is linked to the fusiform face area of the inferior occipitotemporal cortex, usually bilaterally or on the right.
Astereognosis, or tactile agnosia, is the inability to identify a common object such as a coin or a key placed in the hand with the eyes closed, despite intact touch, pain and position sense; it points to the contralateral parietal association cortex.
Anosognosia is the denial of a deficit, most classically a patient with a dense left hemiplegia from a right middle cerebral artery stroke who insists nothing is wrong; it accompanies left hemineglect and is the single most dangerous agnosia on a ward because the patient tries to walk.
Finger agnosia belongs to Gerstmann syndrome, which is finger agnosia, agraphia, acalculia and left-right disorientation together, and localises to the angular gyrus of the dominant parietal lobe.
Auditory agnosia is the failure to recognise non-verbal sounds such as a telephone or a barking dog with normal hearing, and follows bilateral superior temporal lesions.
Agnosia must be distinguished from three neighbours: aphasia is a disorder of language, apraxia is the inability to carry out a learned movement despite normal power and comprehension, and anomia is the failure to name an object that is otherwise recognised.
The usual causes are stroke in the posterior cerebral or middle cerebral territory, head injury, tumour and neurodegeneration, including the posterior cortical atrophy variant of Alzheimer disease.

Ear — anatomy

The ear is a single organ serving two senses: hearing and balance. It is built in three parts, an external ear that collects sound, a middle ear that is an air-filled cavity converting air-borne vibration into mechanical movement through three tiny bones, and an inner ear whose fluid-filled labyrinth contains the cochlea for hearing and the vestibular apparatus for equilibrium, all served by the eighth cranial nerve.

The external ear is the auricle of elastic cartilage, whose lobule contains no cartilage, and the external acoustic meatus, about 24 mm long, with a cartilaginous outer third bearing hair and ceruminous glands and a bony inner two-thirds.
The tympanic membrane is a pearly grey, obliquely set membrane about 9 to 10 mm across with the handle of the malleus visible and a cone of light in the anterior-inferior quadrant; it separates the external from the middle ear.
The middle ear contains the three ossicles in sequence, malleus, incus and stapes, with the footplate of the stapes in the oval window; the stapes is the smallest bone in the body, and the tensor tympani (trigeminal nerve) and stapedius (facial nerve) damp them in the attenuation reflex against loud sound.
The ossicular chain and the difference in area between the tympanic membrane and the oval window amplify the sound pressure roughly twenty-fold, which is what allows vibration in air to move fluid in the inner ear without being lost.
The pharyngotympanic (Eustachian) tube joins the middle ear to the nasopharynx and equalises pressure across the drum; in a child it is shorter, wider and more horizontal, which is why acute otitis media is so much commoner in children and why it follows upper respiratory infection.
The facial nerve runs in a bony canal in the medial wall of the middle ear and along the mastoid, so it is at risk in chronic middle ear disease and in mastoid surgery; the chorda tympani branch crosses the cavity carrying taste from the anterior two-thirds of the tongue.
The inner ear is a bony labyrinth containing perilymph and, suspended within it, a membranous labyrinth containing endolymph; the cochlea houses the organ of Corti on the basilar membrane for hearing, while the utricle and saccule detect linear acceleration and gravity and the three semicircular canals, set at right angles to one another, detect angular acceleration.
Tuning fork tests use this anatomy: in Rinne's test air conduction normally exceeds bone conduction, while Weber's test lateralises to the diseased ear in conductive deafness and to the better ear in sensorineural deafness.

Anosmia

Anosmia is the complete loss of the sense of smell, and hyposmia is its partial loss; both are disorders of the first cranial nerve or of the nasal passage that leads to it. It matters far beyond the loss of pleasure, because most of what people call taste is smell, and because a sudden anosmia can be the first sign of a cribriform plate fracture, a frontal lobe tumour or a neurodegenerative disease.

The olfactory receptor neurons lie in the olfactory epithelium in the roof of the nasal cavity, over the superior concha and the upper part of the septum; their unmyelinated axons pass as about twenty filaments through the cribriform plate of the ethmoid bone into the olfactory bulb, and then run in the olfactory tract to the piriform and entorhinal cortex and the uncus of the temporal lobe.
Olfaction is the only sensory modality that reaches the cerebral cortex without first relaying in the thalamus, and its close link with the limbic system is why smells trigger memory and emotion so strongly.
Conductive causes block odorant molecules from reaching the epithelium: the common cold, allergic rhinitis, chronic rhinosinusitis, nasal polyps and a grossly deviated septum; these are usually reversible.
Sensorineural causes damage the receptors or their filaments: post-viral anosmia including after COVID-19, head injury that shears the olfactory filaments as they cross the cribriform plate, ageing, smoking, occupational toxins and some drugs.
Head injury with anosmia and a clear watery discharge from the nose means a cribriform plate fracture with a cerebrospinal fluid leak, which carries a real risk of ascending meningitis; the fluid gives a halo or target sign on a tissue and tests positive for glucose, and beta-2 transferrin confirms it.
Anosmia is an early, sometimes pre-motor, feature of Parkinson disease and of Alzheimer disease, appearing years before the movement disorder or the memory loss.
Kallmann syndrome is anosmia with hypogonadotropic hypogonadism, caused by failure of the olfactory and gonadotrophin-releasing hormone neurons to migrate together in fetal life, and it presents as delayed or absent puberty with no sense of smell.
An olfactory groove meningioma can give the Foster Kennedy syndrome: ipsilateral anosmia with optic atrophy and contralateral papilloedema, so a unilateral anosmia with visual change is never dismissed.
Test each nostril separately with a mild non-irritant odour such as coffee, cloves or soap while the other is occluded; ammonia and other pungent substances are not a test of the olfactory nerve because they stimulate trigeminal endings.

Auditory pathway

The auditory pathway is the chain of neurons that carries sound from the hair cells of the organ of Corti in the cochlea to the primary auditory cortex in the temporal lobe. It is unusual among sensory pathways because it crosses and re-crosses at several levels, so that each ear is represented on both sides of the brain, and this single fact explains why a stroke never causes deafness in one ear.

The receptors are the hair cells of the organ of Corti resting on the basilar membrane; the inner hair cells are the true sensory receptors that generate the signal, while the outer hair cells act as a mechanical amplifier that sharpens sensitivity and tuning.
First-order neurons are the bipolar cells of the spiral ganglion in the modiolus of the cochlea; their central processes form the cochlear part of the vestibulocochlear nerve, the eighth cranial nerve.
The fibres end in the dorsal and ventral cochlear nuclei at the junction of pons and medulla, and most second-order fibres then cross the midline as the trapezoid body to reach the superior olivary complex of the opposite side, while some stay on the same side.
The superior olivary complex compares the time of arrival and the intensity of sound at the two ears and is where the brain localises where a sound came from.
The pathway then ascends in the lateral lemniscus to the inferior colliculus of the midbrain, which also mediates the reflex turning of the head and eyes towards a sudden sound, and then relays in the medial geniculate body of the thalamus.
Fibres from the medial geniculate body form the auditory radiation and end in the primary auditory cortex on the superior temporal gyrus, in the transverse gyri of Heschl, Brodmann areas 41 and 42, with the auditory association area 22 alongside it and Wernicke's area in the dominant hemisphere.
Because of the repeated crossings, a unilateral lesion above the cochlear nuclei causes at most a subtle difficulty in localising sound and never one-sided deafness; deafness in one ear means the cochlea, the cochlear nerve or the cochlear nuclei themselves.
Tonotopic organisation is preserved from the cochlea to the cortex: the base of the cochlea responds to high frequencies and the apex to low, which is why noise-induced and age-related loss show up first in the high frequencies around 4 kHz.
The pathway is tested objectively by brainstem evoked response audiometry, whose waves I to V correspond to successive relays, and by otoacoustic emissions from the outer hair cells, which together form the newborn hearing screen.

Free today: the 10-question daily quiz · the NORCET 11 recall paper · what ₹999 unlocks — once, no auto-renewal.