The automatic bladder, excessive sweating and some other reflex conditions, in gross injuries of the spinal cord. By Henry Head, MD, FRS and George Riddoch, MD, Captain, Royal Army Medical Corps. (Officer in charge of the Empire Hospital, Vincent Square). Brain 1917; 40: 188–263.
Cambridge
‘The present War has afforded innumerable opportunities for investigating the phenomena due to gross injuries of the spinal cord ...’. After working independently on the manifestations of total transverse section and the explanation for excess sweating as a sequel to spinal cord injury, respectively, Dr Head and Captain Riddoch (Figs 1 and 2) now realize that, in also studying the functional capacity of the automatic bladder, they are looking at different aspects of the same problem; and so they join forces. Based at the London Hospital and the Empire Hospital for Officers, they propose a physiological explanation for the clinical observations made by Dr Riddoch (see Brain 1917; 40: 264–402 and 2004; 129: 2150); and offer a general explanation for the remarkable behaviour of the distal end of the severed spinal cord. They acknowledge the invaluable work of the Cambridge school of physiology (John Langley, [Sir] Hugh Anderson and Thomas [TR] Elliot inter alia) on the involuntary nervous system (summarized and reviewed in the same issue by Dr EG Fearnsides, Brain 1917; 40: 149–87).
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Acute cord section results in urinary retention and, if complicated by infection and bed-sores, carries a high early mortality. After 2–3 weeks—sooner with partial cord injury and later when there is concomitant damage to the cauda equina—survivors usually develop automatic bladder emptying. Head and Riddoch aim to show that this partially restored function and other reflex activities to be discussed, depend on extra-vesical stimuli. First, in chronic but stable cases, they measure the capacity of the gently distended bladder and show that, in Case 1 studied at 158 days, small oscillations causing slight increases of pressure are seen immediately that increase in amplitude at volumes greater than 400 ml until complete reflex voiding occurs in three phases at 600 ml. Case 1 is neither aware of nor able to influence these activities. At Day 266, Case 1's bladder capacity has reduced to 200 ml and partial reflex emptying can be triggered at even lower volumes by tickling the (insensible) sole of his foot or the glans penis. Similar observations are made in Case 2, studied at 218 days after complete cord section at D4. It is apparent from observations in Case 3, studied at 31 and 60 days, that the effect of respiration is not merely to induce mechanical pressure wave oscillations on the bladder but also to stimulate reflex voiding of larger amounts at volumes well short of his maximal capacity.
Case 6 has a lower lumbar cord transection and retains the sensation of bladder fullness ... ‘I have a pleasant desire to make water, just as I had when my bladder was full before I was hurt’ ... but still empties by reflex at around 100 ml or less when his insensitive anal skin is pricked, whereas stimulation of skin having preserved sensation has no such effect. Case 8 has a Brown-Sequard syndrome: he is aware of bladder fullness and empties reflexly with pleasure but has no desire to micturate; stimulating the anaesthetic left foot provokes reflex emptying whereas the sensitive right sole has no such effect. At 34 days, Case 7, with damage to the cauda equina, has no reflex bladder emptying other than that evoked by respiration and stimulation above the lesion.
Although scratching the sole of his foot does achieve near-complete reflex emptying in Case 1, without a catheter in situ, co-ordinated contraction of the detrusor with inhibition of the internal urethral sphincter, as in normal micturition, is clearly more vulnerable than reflex detrusor activity with an artificially open sphincter ... ‘the early return of tone to the sphincter mechanism compared with the later recovery of detrusor activity gives the sphincter a dominance that is overcome only under the most favourable conditions’. Although the capacity of the bladder in cases of dorsal or cervical cord injury tends to reduce with time, and especially in the context of infection, expulsion of urine in response to the rising endo-vesical tension may pause briefly with accommodation of a little more fluid, as in normals who can—for a while—resist the urge to micturate; and this is especially likely to occur when activities of the detrusor and sphincter are not synchronized. Against this background, capacity is invariably compromised by fever—often by more than 50%; alternatively, reaching a steady state may be much delayed with an ensuing state of prolonged atony, and increase in the sensitivity and size of the cutaneous zone capable of eliciting reflex emptying.
Of course, it follows that facilitation of the vesical reflex, when present, is also associated with over-reactivity of flexor spasms and tendon reflexes. Less intuitive is the observation that stimulation—without awareness on the patient's part of either the sensation or any involuntary movements—evokes profuse sweating, sometimes above the lesion, limited to an area which is constant in each case and determined by the site of the cord injury. In cervical cases, it affects the head, arms and trunk to the umbilicus; as the site of the lesions descends, so too does the affected area now with the anaesthetic regions more intensely involved. The sweats may be drenching, soaking blankets and pillows, and sufficient to cause thirst and reduced urine volume; and, as a rule, sweating forms part of the reflex syndrome of bladder emptying and flexor spasms especially when the latter are ‘massive’ and have lost their local ‘signature’. The most provocative stimuli include bladder fullness itself, interrupted emptying by a plug of debris, prior damage to the sphincter from traumatic catheterization such that inhibition is uncoupled from detrusor activity, flatulence, or administration of a rectal enema. The extent and distribution of sweating increase with ambient temperature, fever and the administration of aspirin. In Case 8, the pleasurable ‘thrill’ or ‘shiver’ associated with unimpeded micturition is replaced by an unpleasant ‘nervous wave, which seems to start in his abdomen, and pass up to the head and down his arms’ when temporary urethral obstruction induces a bout of reflex sweating. ‘It is now universally recognized that the secretion of sweat is brought about by the sympathetic system, and the connector fibres, conveying these motor impulses to the sympathetic chain, pass from the central nervous system by way of the anterior ... second thoracic and third lumbar roots’. But, although it is only stimulation below the lesion that most reliably induces sweating, this may nevertheless be experienced in the upper and still sensitive limbs and trunk.
How can everything be explained? Riddoch and Head align themselves with the school of experimental and clinical observation that has as its predecessors John Hughlings Jackson, (Sir) Charles Sherrington and (Sir) Francis Walshe. Sherrington has established that physiological reflexes elicit a type-reflex in which the (motor) reaction relates to the site and nature of the (scratch) stimulus giving signature and purpose to the response in place of the diffuse mass-reflex seen when lower mechanisms, i.e. spinal, are set free from descending control. Thus, in spinal cord injury only a vestige of the type-reflex occurs as this is replaced by a stereotyped response to stimulation, wherever placed or however intense—‘... the energy overflow[ing] into channels with which the reflex manifestations are not associated normally’ in the domains of flexor spasms, bladder emptying and sweating.
Perhaps attention to cases that fail to show the mass-reflex may prove instructive. Foremost are those who exhibit reflex extensor posturing to cutaneous stimulation; they never have mass-reflexes involving bladder and sweating. Again, this clinical observation draws on Sherrington's account of the extensor thrust in spinal cord injury of the dog in which alternate flexion and extension of the two limbs amounts to a stepping response that depends on the preservation of proprio-spinal reflex circuits allowing altered muscle tone in response to changes in posture; since these depend ultimately on activity in the semi-circular canals, the appearance of extensor spasms implies some continuity of connection between the midbrain and spinal cord, and yoking of pathways innervating the upper and lower limbs even if the responses of the former are voluntarily controlled. Therefore ‘the massive flexor response ... after complete transection of the spinal cord, is not part of normal postural reflexes but belongs to the ancient nocioceptive mechanism. It has nothing to do with standing or walking. Its nearest ally among the reflexes is not primary extension, but evacuation of the bladder and rectum’.
Even when extensor responses are possible, protective reflex withdrawal to pain may still occur; but now the associated bowel and bladder emptying and sweating, that can be caricatured as a protective fear response, are no longer seen. And it is the experimental work of Sherrington that reminded a sceptical neurological community of the veracity of Hughlings Jackson's teaching from 1864 that positive symptoms result from the removal of control normally exercized by higher over lower centres, a concept given contemporary focus by Walshe's work concluding that reflex flexion of the paralysed lower limb, of which dorsal movement of the hallux is the most easily induced, is a response to noxious or harmful stimuli and defensive rather than related to spinal stepping (Brain 1914–15; 37: 269–336). Simply stated, the position of Drs Head and Riddoch is that if extensor posturing can be obtained, connectivity exists between the midbrain and distal cord even when all movement, sensation and sphincter control appear to be lost and the mass-reflex does not occur. Conversely, even in the presence of some retained sensation and movement, reflex facilitation of the automatic bladder and profuse sweating will not occur if the proprio-spinal circuits remain under higher influence. And although they take as their authority Sherrington's Integrative action of the nervous system (1906), ‘we cannot close this paper without showing how we stand in relation to the work of the French authorities’. But this is barbed admiration. For they proceed to quote the confusion and Francophonic squabbling between Joseph Babinski, Pierre Marie and Charles Foix that followed the description of an ‘extensor plantar response’ as pathognomic for pyramidal affection on the basis of erroneous French amalgamer of flexor and extensor movements, mass-reflexes and sequences endowed with local signature each as automatic actions of the isolated spinal cord.
Dr Head and Captain Riddoch conclude their weighty paper with a detailed account of the eight illustrative cases on which their opinions are based. Conditioned by 90 years of reflection, historical analysis, poetic and literary rendering, and artistic and archival imagery of events that changed irreversibly a world of Empire and industrial revolution, one is still struck by the poignancy of these once physically able and expectant young men whose lives are no less shattered than their spinal cords: Lieutenant M, aged 28, wounded by shrapnel on August 6, 1916 causing total division of the spinal cord at D6—paralysed, anaesthetic, without extensor posturing and subject to mass-reflexes; Private H, aged 24, wounded in France and with complete transection of the cord at D4—paralysed, anaesthetic, without extensor posturing and subject to mass-reflexes; Captain F, aged 29, wounded on April 6, 1917 with complete cord section at D4—paralysed, anaesthetic, without extensor posturing and subject to mass-reflexes; Captain P, aged 30, caught by machine gun fire on October 2, 1916 with partial cord injury at D4—paralysed and anaesthetic but with ipsilateral stepping and crossed extensor posturing but not experiencing mass-reflexes; Air Mechanic H, aged 23, experiencing fracture dislocation of the cervical spine in an aircraft accident—paralysed but not completely anaesthetic, without extensor posturing and subject to mass-reflexes; Private M, a marine aged 38, falling down stairs on board ship and with damage to the lower cord—paralysed and anaesthetic but aware of bladder fullness and subject to mass-reflexes stimulated by eliciting the anal reflex; Gunner P, aged 21, wounded on August 14, 1917 with damage to the cauda equina—paralysed and anaesthetic with neither extensor posturing nor subject to mass-reflexes; and Lieutenant G, aged 24, wounded by shrapnel from an explosive shell with partial left sided lower cervical cord damage—a Brown-Séquard syndrome with extensor posturing and no mass-reflexes on stimulation of the left leg but flexion and facilitation of automatic bladder emptying and sweating on irritating the right (Fig. 3).
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Their subsequent histories are not known but these eight soldiers had no prospects for recovery. Nor could their successors injured in subsequent conflicts or civilian accidents resulting in spinal cord injury hope for better. Now (see page 2240 and 2376), Alan Mackay-Sim and colleagues from Brisbane (Australia) put a (still paralysed) foot in this door of hopelessness, building on their previous account of the surgical procedure (Brain 2005; 128: 2951–60), to show that stereotactic olfactory ensheathing cell transplantation in spinal cord injury is safe, at 3 years, and so can now be studied more intensively for efficacy in further trials.
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