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Lesions of the C4 or C5 segments of the spinal cord, if complete, will interrupt suprasegmental control of both the sympathetic and sacral parasympathetic nervous systems Much the same effect is observed with lesions of the upper thoracic cord (above T6) Lower thoracic lesions leave much of the descending sympathetic out ow intact, only the descending sacral parasympathetic control being interrupted Traumatic necrosis of the spinal cord is the usual cause of these states, but they may be due as well to infarction, certain forms of myelitis, and tumors As discussed in greater detail in Chap 44, the initial effect of an acute cervical cord transection is abolition of all sensorimotor, re ex, and autonomic functions of the isolated spinal cord The autonomic changes include hypotension, loss of sweating and piloerection, paralytic ileus and gastric atony, and paralysis of the bladder Plasma epinephrine and NE are reduced This state, known as spinal shock, lasts for several weeks The basic mechanisms are not known, but changes in neurotransmitters (catecholamines, endorphins, substance P, and 5-hydroxytryptamine) are under investigation After spinal shock dissipates, sympathetic and parasympathetic functions return, since the afferent and efferent autonomic connections within the isolated segments of the spinal cord are intact, although no longer under the control of higher centers With cervical cord lesions, there is a loss of the sympathetically mediated cardiovascular changes in response to stimuli reaching the medulla However, cutaneous stimuli (pinprick or cold) in segments of the body below the transection will raise the blood pressure However, a fall in blood pressure is not compensated by sympathetic vasoconstriction Hence tetraplegics are almost obligatorily prone to orthostatic hypotension Pinching the skin below the lesion causes goose esh in adjacent segments Heating the body results in ushing and sweating over the face and neck but not the trunk and legs Bladder and bowel, including their sphincters, which are at rst accid, become automatic as spinal re ex control returns There may be re ex penile erection or priapism and even ejaculation With lesions in the upper thoracic cord, similar but lesser degrees of labile blood pressure are seen; in several of our patients with destructive myelitis, a viral infection of fever brought out episodes of a drop in blood pressure to approximately 80/60 mm Hg and a subsequent rapid rise to 190/110 mmHg After a time the tetraplegic may develop a mass re ex (page 1052), in which exor spasms of the legs and involuntary emptying of the bladder are associated with a marked rise in blood pressure, bradycardia, and sweating and pilomotor reactions in parts below the cervical segments (autonomic dysre exia) These reactions may also be evoked by pinprick, passive movement, con-.

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Acute Autonomic Crises (Sympathetic Storm)

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Several toxic and pharmacologic agents such as cocaine and phenylpropanolamine are capable of producing abrupt overactivity of the sympathetic and parasympathetic nervous systems severe hypertension and mydriasis coupled with signs of CNS excitation, sometimes including seizures Tricyclic antidepressants in excessive doses are also known to produce autonomic effects, but in this case there is cholinergic blockade, leading to dryness of the mouth, ushing, absent sweating, and mydriasis The main concern with tricyclic antidepressant overdose is the development of a ventricular arrhythmia, also on an autonomic basis, presaged by prolongation of the QT interval on the ECG Poisoning with organophosphate insecticides (eg, Parathion), which have anticholinesterase effects, causes a combination of parasympathetic overactivity and motor paralysis (see page 1037) A severe degree of autonomic disturbance, involving both postganglionic sympathetic and parasympathetic function, is produced by ingestion of the rodenticide N-3-pyridylmethyl-N -p-nitrophenylurea (PNU, Vacor) The exaggerated sympathetic state that accompanies tetanus manifest by diaphoresis, mydriasis, and labile or sustained hypertension has been attributed to circulating catecholamines Among the most dramatic syndromes of unopposed sympathetic-adrenal medullary hyperactivity occur in the context of severe head injury and with hypertensive cerebral hemorrhage Three separate mechanisms of the hypersympathetic state are observed at different times after the injury or cerebral hemorrhage: an outpouring of adrenal catecholamines at the time of the ictus with acute hypertension and tachycardia; a brainstem-mediated vasopressor reaction (Cushing response, described below); and a later phenomenon, consisting of extreme hypertension, profuse diaphoresis, and pupillary dilation, usually arising during episodes of several minutes duration of rigid extensor posturing (the diencephalic autonomic seizures of Pen eld, described below and in Chap 35 in relation to head injury) Regarding the rst type of sympathetic response, experimental evidence suggests that nuclei in the caudal medullary reticular formation (reticularis gigantocelluraris and parvicellularis) can precipitate severe hypertensive reactions These nuclear centers are tonically inhibited by the nucleus of the tractus solitarius (NTS), which receives afferent input from arterial baroreceptors and chemoreceptors Bilateral lesions of the NTS therefore produce extreme elevations in blood pressure, and this abrupt rise plays a role in the genesis of neurogenic pulmonary edema (see page 488) These sympathetically mediated effects are eliminated by sectioning of the cervical spinal cord and by alpha-adrenergic blockade The Cushing response, re ex, or reaction, as Cushing described it, occurs as a result of an abrupt increase in intracranial.

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tex These points, already touched upon in this chapter, are elaborated in the following three chapters

The diagnostic considerations in cases of paralysis can be simpli ed by utilizing the following subdivision, based on the location and distribution of the muscle weakness: 1 Monoplegia refers to weakness or paralysis of all the muscles of one leg or arm This term should not be applied to paralysis of isolated muscles or groups of muscles supplied by a single nerve or motor root Hemiplegia, the commonest form of paralysis, involves the arm, the leg, and sometimes the face on one side of the body With rare exceptions, mentioned further on, hemiplegia is attributable to a lesion of the corticospinal system on the side opposite to the paralysis Paraplegia indicates weakness or paralysis of both legs It is most often the result of diseases of the thoracic spinal cord, cauda equina, or peripheral nerves, and rarely, both medial frontal cortices Quadriplegia (tetraplegia) denotes weakness or paralysis of all four extremities It may result from disease of the peripheral nerves, muscles, or myoneural junctions; gray matter of the spinal cord; or the upper motor neurons bilaterally in the cervical cord, brainstem, or cerebrum Diplegia is a special form of quadriplegia in which the legs are affected more than the arms Triplegia occurs most often as a transitional condition in the development of or partial recovery from tetraplegia Isolated paralysis of one or more muscle groups Nonparalytic disorders of movement (apraxia, ataxia, etc) Muscular paralysis without visible changes in motor neurons, roots, or nerves Hysterical paralysis

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