THE DIAGNOSIS OF NERVOUS DISEASESBy A. D. LEIGH, M.R.C.P.

Registrar, The Maudsley Hospital; One-time First Assistant, Department of Neurology andPsychiatry, The London Hospital

The general principles discussed in theprevious article may now be applied to thediagnosis of specific nervous diseases.

I. -Motility DisordersMotility disorders may be considered under

four main groups :

(a) Spastic disorders of movement.(b) Flaccid disorders of movement.(c) Transient disorders of movement.(d) Involuntary movements.

(a) Spastic motility disordersRelease of the spinal centres and certain

brain stem nuclei from cortical control resultsin the disturbance of muscle tone known asspasticity. Depending on the site of the lesion,one may consider a cerebral group of spasticpalsies, and a spinal group.The cerebral spastic palsies may be hemi-

plegic, affecting one side of the body; dip-legic, affecting both sides of the body, es-pecially the lower limbs; and monoplegic,affecting chiefly a single limb. Owing to thelarge extent of the motor cortex a monoplegiais usually indicative of a cortical or subcorticallesion. In the internal capsule the fibres areso crowded together that a lesion here pro-duces a hemiplegia.. If there is a bilaterallesion-most commonly at a cortical or sub-cortical level, a diplegia results.

Given a cerebral spastic palsy, the differ-en'tial diagnosis largely depends on the tem-poral factor-the acuity or chronicity of theprocess, its congenital or acquired character.Under the eponym of Little's disease are in-cluded those cases of hemiplegia or diplegia ofpre-natal origin; a history of palsy sincebirth is diagnostic.

Of the acquired cerebral spastic palsiesthose of acute onset during adult life are mostusually vascular in origin-the result of throm-bosis, embolism or haemorrhage. Primaryinfections of the nervous system, such as acutedisseminated encephalomyelitis, or acute dis-seminated sclerosis are relatively uncommoncauses. Neurosyphilis and head injury maybe excluded by relevant investigations.

Chronic and progressive hemiplegia is ofquite different etiology. A neoplasm, eitherprimary or secondary, is the commonest cause,followed by cerebral abscess, tuberculoma or,extremely rarely, gummatous formation.The spinal spastic palsies, resulting from

lesions of the pyramidal tract at a spinal level,form a large group of neurological disorders.Paraplegia of congenital origin is a rarity; inchildhood acute paraplegia may result fromthe disseminated encephalomyelitis of fevers,notably following measles, mumps, andvaccination. A commoner cause however, isPott's disease, and here the paraplegia may beacute or subacute in onset, the latter beingmost usual.

In adults disseminated sclerosis holds prideof place, with trauma, syphilis, and acutetransverse myelitis of unknown origin enteringinto the differential diagnosis. A sudden pro-lapse of an intervertebral disc must be re-membered as a cause of acute paraplegia.

Chronic and progressive spinal spasticpalsies form the largest group of paraplegias-beginning as a paraplegia in extension andwith progression to a complete transverselesion becoming a paraplegia in flexion. Dis-seminated sclerosis, neoplasnms of cord, roots orvertebrae, motor neurone disease, syringo-melia, syphilis, and the hereditary disordersmust be considered, with the emphasis on theexclusion of cord compression:

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(b) Muscular atrophies and flaccid palsiesIn contrast to the preceding group the ' final

common path' is the epicentre of the dis-turbance. Lesions of the anterior horn cell,anterior root, and peripheral nerves may allproduce muscular atrophy and flaccid motilitydisorder. The characteristic objective findingsare muscle wasting, motor palsy or paresis,diminished or absent tone and reflexes.

In infancy two conditions of rare occurrencemay be encountered, amyotonia congenita andthe Werdnig-Hoffman syndrome. The for-mer is characterized by gross loss of power,with flaccidity, with no wasting; the latter bymuscular atrophy similar in distribution to theprogressive muscular atrophy of adults.

In childhood and adult life the two commoncauses of an acute flaccid palsy are acuteanterior poliomyelitis and, less commonly, anacute toxic polyneuritis. The history,^ thesymmetry of the process, and the spinal fluidfindings are diagnostic.

Chronic flaccid motor disorder may resut,from disease of anterior horn cell, nerve rooltsperipheral nerves and muscle.(i) Neuronal disorder most commonly occurs

with progressive muscular atrophy,medullary neoplasms, and with syringo-myelic cavitation. Amyotrophy, fascicula-tion and fibrillation, and the asymmetryof the signs are of value diagnostically. Inboth conditions pyramidal disturbancemay be observed.

(ii) Disorders of roots and nerves are to bedistinguished by sensory change in derma-tome or glove and stocking distribution,by the symmetry of the clinical picture,and by the distal distribution of themuscular weakness. All types of poly-neuritis may be encountered, the com-monest being diphtheritic in origin. Rarerforms include:(i) Peroneal muscular atrophy, a heredo-

familial disorder, affecting mostseverely the motor fibres of the nervetrunks, in particular the peronealnerves. Foot drop, with wastingcreeping up the limb to give the' stork-leg' appearance, followed bywasting of the hand and forearm,occurs characteristically in anadolescent patient.

(2) Progressive hypertrophic polyneuritis,where the essential diagnostic con-sideration is gross thickening of thenerve trunks.

(3)ILeprosy-again associated with thick-ened nerves and perhaps dermalmanifestations.

(iii) Disorders of muscle are distinguished bythe selective nature of the process, pro-gressive wasting and weakness occurringin certain muscle groups. Beginning inchildhood or early adult life, affectingseveral siblings, there heredo-familial dis-orders are manifested by a mixture ofatrophy and hypertrophy of proximalmuscles (hip and shoulder girdles), ab-sence of fasciculation and fibrillation, or ofsigns of nervous system disease. A ratherartificial nosology includes :-

(I) Pseudo - hypertrophic muscular dys-trophy, where the increased bulk ofthe muscles is the presenting feature.

(2) Erbs juvenile dystrophy-manifestedby simple weakness and wasting of hipand shoulder girdle muscles.

(3) The Landouzy-Dejerine type of, dys-trophy-with facial, scapulohumeral,and sternomastoid muscles selectivelyaffected.

(c) Transient or recurrent palsiesTwo uncommon epileptic manifestations,

'Todds paralysis,' and ' inhibitory ' or akineticattacks, are to be considered in this group. Theformer follows immediately upon a generalizedepileptic attack. Although commonly hemi-plegic in distribution, the weakness mayaffect one limb only. The palsy is usually ofonly a few hours duration, rarely persisting fora day or two. Full recovery of function alwaysensues.

'Inhibitory epilepsy' was first described byGowers and Jackson, transient loss of functionbeing the sole manifestation of the attack.The cataplectic attacks which occur in

association with narcolepsy are an unusualcause of recurrent transient palsy. In additionto the characteristic sleep attacks, suddenaccesses of muscular weakness result from

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emotional reactions such as laughter, excite-ment or fear. The patient may fall to theground, but consciousness is invariably pre-served.

In familial periodic paralysis metaboliccrises result in recurrent attacks of flaccid'paralysis. Heredo-familial in nature and be-ginning about puberty, the paralysis usuallydevelops during sleep. The patient wakes inthe morning to find himself more or less com-pletely paralysed. Consciousness is never im-paired. The weakness begins in the hipmuscles and spreads upwards, the musclesshowing a striking loss of irritability both tomechanical and electrical stimuli. The attackmay last for a few hours to several days, andis considered to result from a disorder ofpotassium metabolism.

Myasthenia gravis is characterized by ab-normal' fatiguability and weakness of thestriated muscles, particularly the ocular, faciai,pharyngeal and laryngeal musculature. Theweakness later becomes generalized. Theresponse to prostigmine has attained diagnosticvalue, and an injection of 2.5 mgms. of prostig-mine should always be used as a therapeutictest. Finally, hysterical weakness or paralysismust be considered. The absence of objectivesigns of a lesion of the nervous system, and thepsychiatric findings are conclusive.

(d) Involuntary movementsSix main types of involuntary movements

may be recognized, viz., tremors, choreicmovements, athetotic movements, torsionspasm, tics, and myoclonic movements.

(i) TremorBy tremor is meant an involuntary

rhythmical oscillation around the point ofequilibrium of the affected part. It maybe confined to the head, upper or lowerlimbs, or may be generalized. So diverseare the mechanisms responsible thatneurological classification is extremelydifficult and for practical purposes adivision may be made according to therange of movement into:-(I) fine tremors with rapid small oscilla-

tions, and(2) coarse tremors with slower oscilla-

tions.Into the first group falls the tremor

occurring with thyrotoxicosis, and withintoxications such as mercury, lead, mor-phine and alcohol. A frontal neoplasmmay produce a fine tremor in the upperlimbs of the same or of the oppositeside.

In the second group may be includedthe tremor of paralysis agitans and ofhepatolenticular degeneration.

Intermediate between the two groups isthe rather coarse tremor of hands andface, especially the lips, which is foundin G.P.I.A word might be said here concerning

intention tremor,' the characteristicfeature of which is the accentuation of the'tremor' by movement. By definition itis not a tremor, but'an ataxia--a defect inco-ordination resulting from proprio-ceptic impairment, whether on the cere-bellar or the sensory pathways. The twotypes of ataxia may be distinguished bythe preservation or otherwise of positionsense.

(ii) Choreic movementsThese sudden, jerky, irregular, in-

voluntary movements of semi-purposivecharacter, involving the face, trunk andextremities, are symptomatic of lesions inthe region of the basal ganglia. In child-hood they form the presenting feature ofSydenham's chorea; sporadic cases ofencephalitic lethargica may also showchoreic movements. In adult lifeHuntington's chorea must be considered,the chronic and progressive course withassociated dementia being diagnostic ofthis condition. Vascular lesions and neo-plasms of basal ganglia and superiorcerebellar peduncle are encountered moreinfrequently.

(iii) AthetosisAthetotic movements are closely allied

to choreic movements, and transitionalforms are termed choreoathetotic. Incontrast, however, the athetotic move-ments are slow, writhing, irregular and in-voluntary, being most marked in theupper limb.' In early life they are com-monly encountered in cases of Little'sdisease, and in certain rare degenerative

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affections. In later life following attacksof encephalitis lethargica, vascular insultsand basal neoplasms.

(iv) Torsion spasmSpasmodic twisting and turning move-

ments of the body, especially of theproximal muscles of hip and shouldergirdles occurs in a variety of extrapyramidal syndromes. It seldom occursapart from other niovements such aschorea or athetosis, and is found inpatients suffering from hepatolenticulardegeneration, encephalitis lethargica andcertain congenital disorders.

(v) The ticsA tic may he defined as a ' sudden, brief

irresistible movement, resulting in theinvoluntary contraction of one or moremuscles and representing some act for aparticular purpose.'They may be derived from habits, may

be grafted on pre-existing choreic move-ments, or may be associated with mentalconditions such as obsessive compulsivestates. Tic-like movements are a wellrecognized sequalae of encephalitis leth-argica.

(vi) Myoclonic movements.Sudden, local twitching of muscles

occurring most commonly in the upperlimbs and termed the 'jumps' or 'jerks,'is frequently observed in epilepsy. Theymay precede the major attacks or be thetotal representation of an epileptic attack.

II. Disorders of SensationsSensory disturbance may be either sub-

jective, the patient complaining of pain orparaesthesiae, or objective, when the examinermay discover areas of analgesia or hypalgesia(loss or diminution of pain sensibility),anaesthesia or hypaesthesia (with reference tolight touch). There may be excessive re-action to the different stimuli--a hyperalgesiaor hyperaesthesia.Whatever the variety of sensory disturbance,

however, its significance can only be assessedby the consideration of.:-

(a) The nature of the sensory change.

(b) The distribution of the sensory change.(c) The degree of sensory change.The site of the lesion may then be predicted

with considerable accuracy.

(a) Lesions ofperipheral nervesA knowledge of the cutaneous areas supplied

by individual nerves is essential for accuratediagnosis. In general, however, a small areaof analgesia surrounded by a larger area ofanaesthesia is suggestive of. a peripheral nervelesion. Trauma or pressure are the commonestcauses; leprosy is rarely encountered in thiscountry.When there is a generalized affection of

peripheral nerves-a polyneuritis-the sen-sory changes occur symmetrically over thedistal parts of the limbs. The common causesof polyneuritis have been discussed in thesection on flaccid palsies.(b) Lesions of spinal nerve roots

In contrast to a peripheral nerve lesion, witha root lesion the area of analgesia is larger thanthe area of anaesthesia. This is a result of theoverlap of tactile fibres, so that even in ex-tensive lesions of the roots. no change intactile sensibility may be detected. The dis-tribution of the analgesia is in the dermatomesupplied by the root concerned, hence theimportance of,a working knowledge of thedermatome areas.The common root lesions are produced by

tabes, herpes zoster, trauma, or by the effectsof pressure whether from a neoplasm of cord,root or vertebral structure. In recent years aprolapsed intervertebral disc has been recog-nized as one of the commonest causes of rootcompression. A syphilitic radiculitis, as dis-tinct from tabes, may produce root signs.

(c) Lesions of the spinal cordIoss or impairment of all forms of sensation

below a given dermatome is characteristic ofa spinal cord affection. The level of the lesioncan most easily be obtained by testing with thedrag pin, passing from the area of sensorychange to the area of normal sensation. With acentral intramedullary lesion, pain and thermalsensibility are more severely affected thantactile appreciation.

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The common causes of sensory change atthe spinal level are :-(i) Any cause of pressure upon the cord-

whether due to trauma, neoplasm or in-fective process.

(ii) Intramedullary lesions such as syringo-myelia, neoplasms or disseminatedsclerosis.

(iii) Infections of the nervous system pro-ducing a myelitis.

(d) Lesions of the brainA sensory change, over one half of the body

indicates a lesion on the opposite side of thebrain. Whether cortical, subcortical, thalamicor brain stem in situation may be determinedby the nature of the sensory change and thepresence of other neurological signs. Withbrain stem lesions crossed paralyses accom-pany the sensory change. Thus a lesion inthe pons is manifested by a sixth nerve palsyon the side of the lesion and pyramidal andsensory signs on the opposite side.A profound loss of both cutaneous and deep

sensibility is found with a lesion in theneighbourhood of the thalmus. The thalamicsyndrome first described by Dejerine andRoussy includes, in addition to the above sen-sory change, spontaneous pains and an overreaction to certain stimuli such as pain andtemperature, accompanied by choreoathetoidmovements, especially in the contralateralupper limb.

Loss or impairment of the discriminativeaspects of sensation indicates a cortical situa-tion. The maximal sensory change is foundover the hands and feet, and there is oftenlittle change over the trunk. When a change isobserved it can be noted to extend a centimetreor so across the mid line. With a corticallesion there is a great variability in theresponses, as the sensory cortex tires easily.The usual cause of these sensory syndromes

is a vascular insult-commonly a thrombosisor haemorrhage. Neoplasms, primary andsecondary, and the demyelinating diseases(disseminated sclerosis, Schilder's disease, etc.)must be excluded.

III. Attack DisordersSudden, reversible, recurrent disorder of

nervous function occurs in a large number of

conditions of both nervous and systemicorigin. The historv is the most importantdiagnostic agent, as in most cases physicalsigns are equivocal. The age of onset, thecharacter of the attack, and its periodicity arethe most useful criteria.The immature nervous system reacts more

violently to the impact of disease than does themature organization. Hence convulsions ininfancy may have a completely differentsignificance to convulsions occurring in laterlife. In the first few days of life, injury orcongenital defect of the brain are the com-monest cause of convulsions. Between sixmonths and three years tetany, often pre-cipitated by an attack of diarrhoea or a mildinfection, is a potent cause. A convulsion mayusher in an exanthem such as measles or ameningeal infection. When repeated con-vulsions, for which no cause can be discovered,occur in a child, epilepsy must be envisaged as adiagnosis.

During adolescence epilepsy usurps theplace of. tetany and acute infections. Focalattacks with all that they imply, hypoglycaemiccrises, and renal inefficiency begin to assume arole in differential diagnosis.

In adult life episodic attacks of neuraldysfunction usually indicates an epileptic dis-order. The epilepsies remain one of the mostfascinating subjects in neurology, a mirror ofthe most diverse nervous function. In spiteof recent technical advances such as theelectro-encephalogram, there is no substitutefor wide clinical experience.A recapitulation of the diverse clinical

manifestations of epilepsy is .not indicated in apaper of this nature. Suffice it to mentioncertain important features :

(i) An epileptic attack may be considered, inthe words of Hughlings Jackson, as dueto ' occasional, sudden, excessive dis-charges of grey matter.' Depending onthe degree of spread of this discharge, soan attack may remain focal (Jacksonian)or may become generalized.

(ii) This explosive discharge may occur atalmost any level in the nervous system-but is commonest at the cortical level.

(iii) Epilepsy cannot be considered as, adisease sui generis, for it may be the ex-pression of many different conditions-

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renal insufficiency, vascular disease, etc.(iv) A differentiation into essential or idio-

pathic and symptomatic epilepsy is use-ful, although the former group is con-tracting with advances in knowledge.

(v) It is useful to consider an epileptic attackin relation to four sequences in times.First, the prodromal period, with itssignals of an oncoming fit occuring severalhours or days before the attack.Secondly, the aura, which is in effect apart of the attack and immediately pre-cedes loss of consciousness. It is an in-dication of the situation of the dis-turbance. Thirdly, the content of thefit, whatever it may be, and fourthly, thesequalae, sleep headaches, limb weaknessor automatisms.

(vi) Disease of the brain, in the sense thatpathological changes can be detectedpost-mortem, may produce either focal orgeneralized convulsions. In 50 per cent.of patients with a frontal lobe neoplasm,for example, fits occur, and may be quiteindistinguishable from the idiopathicvariety. It is a sound rule that when anattack occurs in a patient over the age of40, disease of the brain must bethoroughly eliminated before diagnosingidiopathic epilepsy.

(vii) Distinction from other paroxysmal dis-orders.(i) Faints, or syncopal attacks may be

extremely difficult to differentiatefrom petit mal attacks. However, therelation of syncope to emotion, painor fatigue, the sweating and nauseawhich precede a faint, and theabsence of incontinence are helpful.In Stokes-Adams's attacks thepresence of heart block is diagnostic.

(2) Menieres Syndrome. Here recurrentattacks of violent vertigo, accom-panied by vomiting, in a person over40, are usually diagnostic. Thetinnitus and nerve deafness, the longduration,of the attack with no im-pafrment of consciousness, are un-mistakable. It must be pointed out,however, that vertigo may be anepileptic manifestation, but it is then

usually accompanied by some cloud-ing of consciousness.

(3) Hysteria may manifest itself by'attacks '-the hysterical fit sographically described by KinnierWilson 'with limbs quivering andbreast heaving, tremulous eyelids andflushed face, the hysteric gives vent tocries, or talks and mutters, resistingany effort to compose her and oftenneeding restraint.' There is no in-continence, the corneal reflex is re-tained as a rule, and the plantarresponse is invariably flexor.

(4) Of the remaining attack disorders,migraine alone requires mention.Here periodic attacks of headacheoccur, usually unilateral, preceded byvisual auras (teichopsia, scintillatingscotomata) and accompanied or end-ing in nausea and vomiting. Hemi-anopic manifestations are well recog-nized as a migrainous phenomenonbut call for intensive investigation toexclude structural changes, in par-ticular angiomatous malformations.

Disorders of ConsciousnessAwareness of the environment is a function

of the whole organism, in particular of thenervous system working as a whole. It isabundantly clear, however, that certain forma-tions of the brain are more concerned thanothers with this state of awareness or 'con-sciousness.' The region surrounding thethird ventricle, in particular the hypothalamus,and the brain stem, especially the mid-brain,are important loci for the maintenance ofconsciousness. Thus diseases affecting thewhole brain or, more strictly, fxcal processesmay both produce impairment of conscious-ness, ranging from mild degrees of confusionto a state of absolute unconsciousness orcoma.

Neurologically, however, we may considerfour main groups of conditions which causeimpairment of consciousness.

(a) TraumaticThe possibility of head injury should be

considered in every unconscious patient, for

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adequate surgery may be life saving. Con-cussion and cerebral contusion account for themajority of cases and call for no special dis-cussion here. Extradural haemorrhage is anurgent indication for operation, and here it iswell to point out that the 'lucid interval' mayvary tremendously from a few minutes toseveral days. It may be altogether absent. Arapidly deepening coma, with spreading signs,following a head injury awakens suspicion.The diagnosis should be made before theclassical Hutchinsonian pupil has appeared.A subdural haematoma may be acute or

chronic in onset, the latter type concerning ushere. Headache, drowsiness and mentalchanges with a history of a fairly recent headinjury form the elements of the syndrome. Animportant feature is the remarkable fluctuationin the signs and symptoms. Diagnosis, how-ever, is not always easy, a history of headinjury may 'not be forthcoming and thesemeiology is widely variable.

Lastly, confusion or coma may result fromfatty embolization of the brain followingtrauma to soft parts or bones. The somaticinjury, skin petechniae, clinical and radio-logical signs of 'bronchopneumonia' and thepresence of fat globules in the sputum andurine are diagnostic.,(b) Toxic and metabolic causes

Alcohol, the barbiturates, the bromides andcarbon monoxide are the commonest toxicsubstances encountered ih practice. Theeffects of alcohol range from the coma of acuteintoxication to the confusion found in Kor-sakow's psychosis. It is important to err onthe side of caution before indicting alcohol asthe sole causal agent of a coma. Carbonmonoxide and the barbiturates are commonlyemployed in suicidal attempts-the circum-stances are often diagnostic.

Bromidism calls for further remark. Thewidespread and often indiscriminate use of thebromides is to be reckoned with when con-fronted by an obscure case of mental confusion.A blood bromide estimation (normal .5-2.5 mgms. per cent.) may be revealing. Valuesbelow Ioo mgms. per cent. may be ignored, butwith levels between Ioo-200 mgms. per cent.symptoms are likely to occur in elderlypatients, or in those with renal or cardio-vascular impairment.

Of the metabolic disorders diabetes mellitus,hypoglycaemic attacks (both spontaneous, andfollowing the use of Insulin) renal impairment,and liver damage may all produce impairmentof consciousness. Two vitamin deficiencystates are of importance-Wericke's en-cephalopathy resulting from a B.I deficiency,and pellagra, a deficiency of several factors ofthe B group. Wernicke's encephalopathy is ofinterest owing to the focal nature of thelesions, which are found in the hypothalamusand upper part of the mid-brain. Drowsinessand confusion are associated with nuclearoculomotor signs, and may occur in anycondition producing a vitamin B.I deficiency--chronic alcoholism, gastric neoplasm, orstarvation.

(c) Vascular disordersCerebral haemorrhage, thrombosis and em-

bolism are banal causes of impairment ofconsciousness. The speed of onset and theprogression are important differential con-siderations.

Subarachnoid haemorrhage results in aclear cut syndrome of sudden onset, severeheadache, neck rigidity, confusion or coma,and a bloody spinal fluid. Finally thrombo-phlebitis of the cerebral venous system,spreading from infected ear, nose or sinuscommonly goes unrecognized.

(d) Diseases of the nervous systemNeoplasm, abscess, acute infections of brain

or meninges commonly impair consciousness.Epilepsy and narcolepsy have been discussedpreviously. It remains to mention somepsychiatric conditions-catatonic stupor, thethe so-called toxic confusional states, andhysterical stupor:

In conclusion, when confronted with theunconscious patient, attention should bedirected to the following:-(i) The colour of the patient, his breathing,

and the smell of his breath.(ii) A careful search for any sign of injury.(iii) Always test the urine, take the blood

pressure and examine the fundi.(iv) Careful exclusion of organic disease before

diagnosing acute alcoholism or epilepsy.

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