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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.

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

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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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accompanied by spasticity, increased re exes, and an extensor plantar re ex (Babinski sign); exceptionally, a small lesion of the motor cortex will not result in spasticity In either event, nerve conduction studies are normal In acute diseases of the lower motor neurons, the tendon re exes are reduced or abolished, but atrophy may not appear for several weeks Hence, before reaching an anatomic diagnosis, one must take into account the mode of onset and duration of the disease Monoplegia with Muscular Atrophy This is more frequent than monoplegia without muscular atrophy Long-continued disuse of one limb may lead to atrophy, but it is usually of lesser degree than atrophy due to lower motor neuron disease (denervation atrophy) In disuse atrophy, the tendon re exes are retained and nerve conduction studies are normal With denervation of muscles, there may be visible fasciculations and reduced or abolished tendon re exes in addition to paralysis If the limb is partially denervated, the electromyogram shows reduced numbers of motor unit potentials (often of large size) as well as fasciculations and brillations The location of the lesion (in nerves, spinal roots, or spinal cord) can usually be determined by the pattern of weakness, by the associated neurologic symptoms and signs, and by special tests magnetic resonance imaging (MRI) of the spine, examination of the cerebrospinal uid (CSF), and electrical studies of nerve and muscle A complete atrophic brachial monoplegia is uncommon; more often, only parts of a limb are affected When present in an infant, it should suggest brachial plexus trauma from birth; in a child, poliomyelitis or other viral infection of the spinal cord; and in an adult, poliomyelitis, syringomyelia, amyotrophic lateral sclerosis, or a brachial plexus lesion Crural (leg) monoplegia is more frequent than brachial monoplegia and may be caused by any lesion of the thoracic or lumbar cord ie, trauma, tumor, myelitis, multiple sclerosis, progressive muscular atrophy, late radiation effect, etc These disorders rarely cause severe atrophy; neither does infarction in the territory of the anterior cerebral artery A prolapsed intervertebral disc and the several varieties of mononeuropathy almost never paralyze all or most of the muscles of a limb The effects of a centrally prolapsed disc or other compressive lesion of the cauda equina are rarely con ned to one leg However, a unilateral retroperitoneal tumor or hematoma may paralyze the leg by compressing the lumbosacral plexus The mode of onset and temporal course differentiate these diseases.

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