doi:10.1093/brain/awt260 Brain 2013: 136; 2928–2932 | 2928 BRAIN A JOURNAL OF NEUROLOGY FROM THE ARCHIVES ‘How the blind dream’ (Abstracts of British and Foreign Journals) – Mr B. G. Johns (The National Review, April 1885) by Samuel Wilks M.D. Brain 1885; 8: 272–3; with A contribution to the pathology of dreams and of hysterical paralysis by Ch. Féré (Physician to the Bicêtre Hospial, Paris) Brain 1887; 9: 488–93; with A contribution to the pathology of night: nocturnal paralysis by Ch. Féré (Médecin de Bicêtre) Brain 1889; 12: 308–25; with Semiology of sleep (Critical Digest) by Dr Paul Blocq, Chef des travaux Anatamo-Pathologiques à la Salpétrière. Translated from the original MS by H.W. Marett Tims M.D. (Edin) Brain 1891; 14: 112–36 Samuel Wilks (1824–1911; see Fig. 1) summarizes a paper in The National Review by (Bennett George) Johns (nk). Since they produce vivid mental visions during sleep, most dreams involve the perception of ‘friends moving about and conversing as in the ordinary real business of life’. It follows that the (congenitally) blind cannot have such dreams; for they know nothing of form or colour that others have gained through stimulation of the retina during life. The blind can only rehearse those impressions to which their intact sensory faculties have allowed access. Any recollections must be limited to touch, hearing or smell. When a blind boy dreams that he is in a field with his dead brother, he knows him by his voice and awareness of the tread and smell of the grass. A blind tramp speaks of a dream as if he is awake but only through hearing and touch. Of particular interest is Mr Johns’ account of a blind man dreaming that he meets a ghost—an apparition and ethereal being that resembles some person known in the flesh but which, being transparent, cannot be seen or felt. A bullet may pass through it without harm; if sitting on a chair, it does not prevent someone else occupying that same seat. Therefore, if the blind can dream of a ghost, it must be through the reduction of all reliable sensations to touch, as Mr Herbert Spencer (1820– 1903) has argued. When Macbeth says that he can see but not feel the dagger, it becomes a ‘dagger of the mind’ (Macbeth: Act 2, Scene 1): ‘Is this a dagger which I see before me / The handle toward my hand? Come, let me clutch thee / I have thee not, and yet I see thee still / Art thou not, fatal vision, sensible / To feeling as to sight? Or art thou but / A dagger of the mind, a false creation / Proceeding from the heat-oppressèd brain?’ Since it seems paradoxical that a blind man can dream of a ghost, Mr Johns tells of a blind person dreaming that he goes to a house where he meets a friend who has been imprisoned: ‘I heard a voice at the door, and I said, “Bless me, if that ain’t John”, and I took him by the sleeve, it was his shirt sleeve I felt, and I was half afeard of him, and surprised he was out weeks before his time. Then ... I dreamt that he tried to frighten me, and make believe he was a ghost by pushing me down sideways, etc., after that I waked and heard no more.’ In this curious state of mind, the blind man recognizes his friend but the latter behaves in such a strange way as to be perceived as a ghost; and, for Samuel Wilks, the ‘pushing him down sideways’ is no ordinary account of how the sighted would get rid of a spiritual being. More enquiries of the blind who dream of ghosts are needed since the well-established effigy, clothed in white and quite impalpable, can scarcely have a place in the blind man’s imagination. Nothing changes: in 2013, a patient experiencing typical left-sided paroxysmal attacks in association with inflammatory brain disease describes a recurring dream in which a ghost passes through her body and into the tingling left arm; she is not frightened because she recognizes, in her sleep, that one of the familiar paroxysms is occurring during the night. Ch(arles) Féré (1852–1907; see Fig. 2) begins his paper on dreams with the assertion that hallucinations during sleep, if reproduced over several nights, are eventually accepted as reality during the day-time, thereby becoming the substance of diurnal delirium and suicidal or homicidal thought ideation. (Hermann) Nothnagel (1841–1905) asserts that dreams trigger epileptic attacks; and the nocturnal ‘fits’ occasionally observed in hysteria may connect with the moral shock that first determined seizures in that patient. Alcohol plays its part. Dr Féré has a patient at the Salpêtrière who, forced to drink to excess by her brothers as a joke, slept only to dream of fantastic animals about to devour her resulting in an hysterical fugue lasting days without waking, that later repeats itself without the provocation of strong drink. Now, he has another case to report. Eugénie P, aged 14 years, attends the outpatient room at the Salpêtrière on 11 September 1886 in the company of her corpulent and quick-tempered mother, and her father who, being in the wine trade, has ‘problems with sobriety’. Overnight on 20 August 1886, Eugénie—whose menstrual periods are of recent onset and irregular—dreams that she is pursued by men through the Place de l’Odéon who want to stab her. She runs as fast as she can and just escapes them. Next day, her mother notices that her legs give ß The Author (2013). Published by Oxford University Press on behalf of the Guarantors of Brain. All rights reserved. For Permissions, please email: [email protected] From the Archives Figure 1 Samuel Wilks (1824–1911). From http://en.wikipedia .org/. Figure 2 Charles Féré (1852–1907). From http://fr.wikipedia .org/. way whilst walking. The dream recurs on subsequent nights. By day she is inattentive and becomes weak in the legs. She speaks of the dream happening whilst she is awake. The men pursue her and call out, seizing her by the hair. She drops objects to prevent the men taking them from her. Her parents can no longer take her for recreational walks because her legs give way. Now she cannot even walk in the house and has a prolonged episode of flaccid weakness of which she appears unaware. Eugénie arrives at the hospital supported by two people. Examination shows facial and Brain 2013: 136; 2928–2932 | 2929 pupillary asymmetry and she has hemianaesthesia with partial loss of hearing, taste and vision on that side; and there is some exaggeration of the tendon reflexes on the right. She has ovarian tenderness. When attempting to walk, her legs go into spasm when each heel strikes the ground; this ‘dicrotism’ is noticeable at every step. Eugénie is prescribed a tonic with bromide and the use of passive exercises whilst she is distracted by reading. Four days later, she has a fit with choking and crying, unconsciousness and incontinence. Thereafter there is gradual improvement so that by 4 October, Eugénie can walk 300 metres unaided from the station in order to attend the hospital. But matters regress when her mother, wishing to go out alone, undresses Eugénie to prevent her from following: there follows much display of passion and wild speaking after which Eugénie lapses into sleep and emerges unable to utter a sound although her understanding is perfect. At the next consultation, Eugénie can produce a few inarticulate words but is unable to write; her tongue has choreiform movements and the gait remains awkward with residual dicrotism. On 18 October her catamenia resumes and matters improve generally although interrupted by a brief episode, precipitated by a nasty fright, of spasm affecting the eyelids and superior rectus muscles so that her eyes roll upwards. By 18 November 1886, Eugénie is again normal other than some slight residual hemianaesthesia. This case bears on the concept of psychical paralysis described by (Sir John) Russell-Reynolds (1828–96) and (Jean-Martin) Charcot (1825–93) in which the motor trouble is precipitated by a mental image of paralysis. The case of Eugénie is one of paralysis through exhaustion of the motor centres following rapid ineffectual discharges insufficient to produce movements—in her case for walking, speaking and writing. In other situations, Dr Féré has been able to produce daytime paralysis by calling forth dreams of running in subjects who are easily hypnotized. They, too, have dicrotic gaits. It follows that ‘dreaming . . . must not be considered as an indifferent phenomenon, but often constitutes the opening scene of a morbid drama, and as such deserves the attention of the physician’. Two years later, Dr Féré reconsiders the relationship of sleep and paralysis, and the poorly understood roles thereon of darkness, inactivity, change in temperature and altered physiological activities, the latter being especially difficult to evaluate. He has already observed that colour and luminosity, which alter at night, influence speech and muscular motion during the daytime: ‘a Mr de B declared that his manner of conversation with Madame De – had changed since she altered the colour of the furniture from blue to crimson’; and Dr Féré has shown that excitations of the muscular force and the circulation diminish on moving from red to violet ambient light. Soldiers find night marches more tiring than those conducted during the day. Smokers cannot tell so well in the dark, either by taste or smell, whether their cigar be lighted or not. Reaction time increases by 7 or 8/100ths second when the eyes are closed. The limbs diminish in volume and show reduced electrical resistance in the dark. The muscular force and volume of the hand seen in hysterics with the eyes closed alter if a large expanse of skin is exposed to light. (Alexander) von Humboldt (1769– 1859) recalls that a ‘Countess of Madrid’ lost her voice at sunset and recovered it at dawn. Some individuals affected by depression of the nervous system experience such profound 2930 | Brain 2013: 136; 2928–2932 functional modifications of their physiology as to be regarded as hibernating. Others have claimed that physiological processes such as childbirth and death from natural causes are more likely to occur at night than during the daytime: ‘but the tolerably numerous data that I have been able to bring together give no evidence of the influence of the night in this respect’. And the lowering of temperature that occurs just before dawn, influencing nervous phenomena, may have its explanation in the observation of the same author that rapidity of the nervous current in the frog reduces from 26 to 15 m/s at temperatures of 0 C. But if physiology alters at night so too do the manifestations of disease. Neuralgia intensifies; and melancholic and hypochondriacal tendencies are experienced at nightfall in neuropathic people. Epilepsy increases in frequency towards the morning. Certain nocturnal mental troubles occur exclusively among overworked men of business. The ancients recognized that darkness is the great nurse of sorrows; and lowering of the eyelids is enough to provoke visual hallucinations in the insane. ‘Vesanic’ (the term introduced in the 1840s for states of cognitive disorganization following insanity) suicides often occur in the morning; but these thoughts of self-destruction may disappear after the victim has taken a stimulant or food. More generally, the overworked are prone to night terrors on waking from terrifying hallucinations that may persist until the dawn breaks; and deprivation of light may provoke nocturnal terror with somatic symptoms, such as angina pectoris and a sense of choking, without any prior mental representation. The influence of the night on sensory and motor functions is profound. In referring to drunkards and impotence, Dr Féré refers not only to general powerlessness at night and on waking but to ‘the member that plays the greatest role in the exercise of their profession’. Night and darkness expose the risk of incontinence: in children too lazy to get out of bed; in those who sleep too soundly to heed the warnings; and in others who dream that they are emptying their bladder appropriately. Dr Féré has shown that the anal sphincter is influenced by light with the sensation of rectal fullness weakened in darkness. Perhaps unrelated is the condition of night blindness or hemeralopia. Not confined to neuropathics with nervous exhaustibility, this is seen as a consequence of disease: in the puerperium; following fatigue in equatorial seas or snow-fields; and in institutions such as prisons or ships and houses of education, where generally it spares the better nourished. One suggestion is that this exhaustion is akin to deafness in people who work in the midst of intense noise. Rather, it seems to Dr Féré comparable to the transitory anaesthesia that may follow sensory paroxysms of epilepsy— an interpretation that he considers commensurate with his previous demonstration of blindness in susceptible individuals, notably hysterics, through wearing red spectacles. Nocturnal blindness is often accompanied by paresis of the (dilated) pupil, difficulties with accommodation, and strabismus; and it improves gradually on waking. But, he has to admit that if nocturnal blindness is a consequence of local or general exhaustion, it occurs under conditions where there is a deficiency not an excess of the physiological excitant. Paresis for want of physiological stimulation is a general feature of hysterics, who typically remain torpid and incapable of movement on waking. The modification of nutrition may explain other morbidities that occur at night. Mr (Silas) Weir Mitchell (1829–1914) has described From the Archives cases of transient paralysis of the arms or one side, with or without painful numbness, on waking; women at the menopause are commonly affected. Mr (Joseph Arderne) Ormerod (1848–1925) has made similar observations; but in his case the disorder is characterized by numbness and prickling severe enough to wake the patient; and with similar symptoms induced in the day by exertion such as washing, rubbing or working with a needle. The condition is particularly prevalent in women at the menopause and relieved by friction of the hands. For Dr Féré, these are examples of nervous exhaustibility consequent upon loss of nocturnal nutrition being ‘the more transitory and less accented troubles that one observes every day, so to speak, in a great number of neurasthenics, and particularly in hysterical people . . . from a sort of transition between normal phenomena of life and those paretic states’. The modern reader would not be alone in differing from Dr Féré, preferring the diagnosis of median nerve compression in the carpal tunnel. Indeed, Mr (Wharton) Sinkler (1845–1910) and Mr (Robert) Saundby (1849–1918) have already attributed these symptoms to position and nerve compression analogous to the disorder of blue discolouration and coldness of the hands [pace Maurice Raynaud (1834–81)]. But Dr Féré offers two illustrative cases that he considers support his formulation of nocturnal nervous exhaustion. Mrs V has had a difficult life: shortly after the death of her husband, with consequent monetary difficulties, she develops constricting head pains likened to constant pressure with a cracking noise in her occiput; her sleep is disturbed by dreadful nightmares of ruin for her entire family; on waking she is unable to move and rise to empty her bladder; her limbs feel numb as if wrapped in cotton; when it becomes light, she has to be coaxed by her mother to get up and helped to dress, at which stage the symptoms gradually resolve over 3 hours; and by day she is uncharacteristically pusillanimous and indecisive. Examination is normal other than pain in the region of the left ovary and numbness on that side. She improves with time and the administration of bromide, hydrotherapy and static electricity. Mrs P has had catamenial migraine for 37 years with scintillating scotomata and other positive visual symptoms that she and Dr Féré describe in meticulous detail. They are unusual in that, with onset of the menopause, she has an intense urge to walk forwards to the extent that all doors and windows in the house must be shut in order to keep her contained. At this stage, she suffers several domestic difficulties: her appetite alters; she has nightmares; she is breathless on exercise and has weary limbs; and her whole spine is painful, tender to the touch and unable to tolerate any pressure. Now she experiences acute pain in the heel and summons a doctor. He suspects gonorrhoeal rheumatism and proceeds to examination of her genitalia. These are considered normal but ‘the examination – the true object of which had been concealed from the patient – provokes very strong excitation, followed by a fit of sadness, out of which it was impossible to rouse her’. Now she sleeps badly and on waking is unable to move her limbs only managing to get up after the application of friction. The episodes become more prolonged and she declares her body to be a ‘pur esprit’. She is admitted to a place of hydrotherapy and undergoes cold douches and, with bromide of potassium, starts to recover. From the Archives In considering these cases, Dr Féré exposes the neuro-erotic preoccupations of his illustrious place of work at that time. He starts, somewhat wildly: these paralyses grow, so to speak, on the same soil as paralyses by exhaustion but instead of being determined by . . . sensorial excitation, or by the mental representation of . . . exhaustion, they are the result of a deficiency of physiological excitation . . . paralyses par inirritation . . . powerlessness by non-irritation can affect all motor and sensorial functions and . . . intelligence in all its manifestations . . . but it is quite useless to insist here on the influence of the immediate surroundings on intellectual development. He explains that, in cases of nocturnal paralysis, ‘it is not only the motility and senses . . . and the cephalic senses which are affected, but the genital sense as well’ . . . ‘for many years I have attended a patient aged 38 belonging to (Bénédict) Morel’s (1809–73) class of dégénerés à stigmates physiques et psychiques . . . who has been incapable . . . of giving himself up to sensual pleasure otherwise than in open air or a lighted room a giorno. He has however, never spared the means of supplying the necessary physiological excitation of light.’ Let us leave Dr Féré and his ruminations and turn to his colleague Paul Blocq (1860–96; see Fig. 3) part of whose treatise subsequently published as Séméiologie et diagnostic des maladies nerveuses [authored with (Jakow) Onanoff (1859–92)] is translated and reproduced as a Critical Digest. Dr Blocq writes of maladies in which sleep is disturbed; and of pathological disorders of sleep itself. Insomnia arises from almost every disease of the brain and its meninges; peripheral excitations such as neuralgia; alterations of the blood; and essential insomnia especially affecting individuals of hereditary nervous temperament. All forms may exhibit excessive twitching. Dreams and visions that could be Figure 3 Paul Blocq (1860–96). From http://baillement.com/. Brain 2013: 136; 2928–2932 | 2931 considered normal and nightmares, which might be designated ‘nocturnal asthma’, are so similar as both to be examples of ‘morbid dreams’. These often precede more obvious manifestations of the underlying disease and reflect the premorbid state in their content: in circulatory disease, dreams are often short and terminate by abrupt wakening; in respiratory disease, the dream is of animals gripping the throat or seated on the chest; disorders of digestion are experienced in dreams as gustatory hallucinations or the sensation of weight on the abdomen; and the nocturnal terrors of children also indicate the probability of intestinal indigestion. ‘But it is most especially in nervous affections that dreaming acquires a semeiological importance.’ Repetition of the same dream indicates ‘signs of degeneration’, the nightmare installing itself and, over years, tormenting its victim. In hysterics, the dreams are followed by paralysis or abasia; and it is notable that in cases of paraplegia, the patient rarely dreams of walking. Some dreams are so constant as to be necessary for establishing the diagnosis. In hystero-traumatism the dream influences subsequent manifestations of the disorder; and other contents are diagnostic, as in the frightful dreams of vermin and infestations of alcoholics. As for pathological disorders of sleep, the three stages of sleeping sickness in west Africa are characteristic: first, droopy eyelids with drowsiness; then, almost permanent drowsiness but with the sufferer still rousable; and, lastly, agonal coma with motor and sensory disturbances. Given the geographical distribution, there is no differential diagnosis; and the same is true of ‘paralysing vertigo’ in Switzerland in which the patient has headache, vertigo, an unsteady gait and bilateral ptosis—all with recovery. Narcolepsy, a pathological exaggeration of the desire to sleep sometimes induced by movement or emotions, is not accompanied by dreaming. On hysterical somnambulism and hysterical apoplexy, Dr Blocq remains loyal to his teacher. Charcot has insisted that these are the same condition, even though the latter is of sudden onset and may be followed by hemiplegia, patients falling in the midst of a conversation or their occupation, then sleeping but without altered respiration and with one or more limbs either limp or rigid. On attempting to open the eyes, there is forced closure with upward movement of the globes; the patients have trismus; are incontinent; unresponsive to physical or electrical stimulation; and show involuntary movements such as opisthotonos or salutation—features that distinguish hysterical somnambulism or apoplexy from narcolepsy and normal sleep. Charcot has taught that there is grand hypnotisme and petit hypnotisme. In the former, the attack starts with lethargy, laryngeal bruit and frothing at the mouth; the lips are closed and the eyelids flutter; and stimulating nerve or muscle results in contraction and withdrawal until antagonists also become active. There follows a cataplectic stage in which the limbs are immobile but remain in the position whence they are placed; and the face mimics posture of the limbs—for example, an ecstatic expression if the hands are placed in a position of prayer. In petit hypnotisme, there are varying degrees of sleep and detachment from the surroundings but the patient always remains in contact with the ‘operator’ and is fully suggestible. Both types can lead to hypnotic somnambulism in which the individual performs activities during sleep. These may be natural, as in sleep walkers, who negotiate objects and come to no harm, with amnesia on waking for everything done during the 2932 | Brain 2013: 136; 2928–2932 episode. In epileptic somnambulism, features of the attack are apparent, usually before onset of the automatic behaviour. But these can be prolonged and not invariably associated with anything to suggest a seizure, making for diagnostic difficulties that may only be reconciled by the response to bromide. Hysterical somnambulism is a transformation of the writhing phase of the hystero-epileptic attack characterized by delirium and hallucinations with marked emotional content, starting with brief convulsive movements and then a prolonged emotionally charged dream which the patient enacts without being in any way suggestible or diverted from the hallucinatory content. Within this definition are people who live in two identities, the actions of the one being unknown to the other and with hysterical physical symptoms confined to a single state. Although not yet fully worked out, there exist cases of traumatic amnesia, similar to the automatic states already described: ‘but their nosographical history is not yet sufficiently made out to warrant their description here. Nevertheless, their eventuality is foreseen, and ideas as to their causation would then establish the diagnosis’. What does the modern reader take from these attempts to apply mechanisms to observed phenomena? Some of the From the Archives descriptions would now be entirely recast as tension headache, somatization disorder, postinfectious polyneuritis (Miller Fisher syndrome), carpal tunnel syndrome and other well recognized conditions. Are we better informed concerning nosological classifications of disease than were neurologists of an earlier generation? Probably, since we apply mechanism-based logic to support our diagnostic formulations; use biomarkers that inform our concepts of pathogenesis; and draw upon evidence from randomized clinical trials. But however off the mark the interpretations proposed by Dr Féré and colleagues may now appear, we should be wary of complacency in assuming that we know more of dreaming and sleep than did neurologists working in 19th century Paris. Dr B.G. Johns and Samuel Wilks thought about the content of dreaming in the blind; and, in the present issue, Smaranda Leu-Semenscu and colleagues raise an equally pertinent issue about the ability to dream when the mind is blank (see page 3076). Alastair Compston Cambridge
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