Complete Text (Part 10)

disease of neck. Signs of intracranial disease present. 1. Paralysis unilateral, at least at first. Lips usually escape. Headache, vomiting and mental dullness common. a. Optic neuritis present, often intense. Pulse often slow. Tumor or Aneurism pressing on medulla. b. Syphilis active; headache chiefly nocturnal. Optic neuritis absent or of slight intensity. Syphilitic Meningitis. 2. Onset always slow, in an adult. Paralysis bilateral from the start, beginning in the tongue, involving the lips and tending to spread to the palate, larynx and pharynx. Headache and optic neuritis absent but optic atrophy may occur. Paralyzed muscles often waste and show altered galvanic reactions even while retaining faradic irritability. Palatal, pharyn- geal and laryngeal reflexes usually lost. May exist alone, but the possibility of its being only part of a widespread degeneration, such as spinal muscular atrophy, amyotrophic lateral sclerosis, tabes, dis- seminated sclerosis or paretic dementia, should always be carefully considered. Typical Bulbar Paralysis^ due to degeneration of nuclei. 3. Onset acute or subacute, usually in a young person. Muscles excessively fatigued when used, but recover BULBAR AND PSEUDO-BULBAR PARALYSIS. 1 27 temporarily after rest. Electrical reactions retained but may be quickly exhausted by repetition of test. No reaction of degeneration, atrophy or sensory symptoms. May extend to masticatory, facial or ocular muscles. Symptoms may vary greatly from day to day. Paralysis of respiration or swallowing may occur, but recovery is possible. Asthenic Bulbar Paralysis^ no anatomical basis known. 128 NERVOUS AND MENTAL DISEASES. LARYNGEAL PARALYSIS. Paralysis of one or more laryngeal muscles without in- volvement of lips, tongue, palate or pharynx and without other indication of organic intracranial disease. I. The neck or mediastinum is so diseased as to damage one or both pneumogastric nerves or their laryngeal branches, e. g.^ stab wound, operation, goitre, enlarged glands, tumor, aneurism, cellulitis, etc. A. The vocal cords move normally in breathing but remain lax on phonation, the glottis forming a wavy line. Food enters the larynx because the epiglottis does not properly cover it. Upper part of larynx more or less anesthetic. Very rare. Bilateral lesion of Superior Laryngeal Nerves. B. One or both cords immovable in cadaveric position (be- tween abduction and adduction). Breathing not im- peded. Phonation and explosive cough equally difficult or (in bilateral lesion) impossible. I. Heart action disturbed; pulse rapid. Respiration may be slow. Vomiting may occur. Lesion of Trunk of Pneumogastric. 2. Pulse and respiration not affected. Lesion of one or both Recurrent Laryngeal Nerves. C. Vocal cords can be adducted in phonation but only partly separated in inspiration. Breathing stridulous, espe- cially during sleep. Partial lesion of Recurrent Nerves. II. There is no disease in the neck or mediastinum, but the larynx is directly injured by the swallowing of injurious substances, by pressure from a lodged bolus, or from adja- LARYNGEAL PARALYSIS. 1 29 cent growths, by syphilitic or catarrhal inflammation, ex- cessive fatigue or the like. Non-nervous Laryngeal Paralysis. III. No nerve lesion or adequate local cause can be found. A. An emotional cause can be traced and symptoms may vary much with emotional changes. History of hyster- ical attacks common and various other signs of hysteria may be present. Paralysis always bilateral. 1 . Voice is reduced to a whisper. Vocal cords do not approach on attempted phonation but move normally in breathing and approach perfectly in explosive coughing or sneezing. May precede or follow hys- terical mutism. Hysterical Aphonia due to paralysis oj" adductors, 2. Voice not impaired. Inspiration stridulous ; expira- tion normal. Very rare. Hysterical Paralysis of Abductors. B. No cause can be found. Paralysis sometimes unilateral. Probably the Jirst symptom of bulbar paralysis or of a widespread degeneration^ such as spinal muscular atrophy^ amyotrophic lateral sclerosis^ tabes^ disseminated sclerosis or paretic dementia. 11 130 NERVOUS AND MENTaL DISEASES. PARALYSIS OF PARTIAL OR IRREGULAR EXTENT. I. The paralysis appears only on attempting certain coordinated movements which have been performed to great excess in the patient's occupation, such as writing, telegraphing, playing a musical instrument, etc. Paralytic form of Writer's Cramf or other Occupation Neurosis, II. All motions requiring the action of the paralyzed muscles equally affected. A. Onset acute, in a few hours to a few days, resembling that of an eruptive fever. Paralyzed muscles waste and lose faradic irritability. No sensory loss. Rheumatoid pains of onset usually quickly subside but may persist. Most cases in later infancy; six-sevenths of all cases under ten years of age. Poliomyelitis, B. Onset acute or subacute, very rarely chronic. Paralysis affects muscle groups supplied by spinal nerves or plex- uses and is accompanied or soon followed by more or less sensory loss in corresponding areas (Figs. 8 to 11). Affected muscles waste and lose their tendon reflexes and faradic irritability. Numb, tingling or burning pain in the affected area with tenderness of the muscles and often of the nerve trunks. Skin often edematous and glossy. I . Paralysis, pain and sensory loss in the area supplied by a single spinal nerve. a. The apparent cause is a wound, pressure on the nerve trunk, exposure, infectious or toxic disease or the extension of adjacent inflammation. Neuritis, b. No traumatic, infectious or toxic cause apparent. Nodular swelling can be felt in the course of the nerve. Neuroma, lUpplied by the brachial, one side. , greatly . Symptoms in tht: e lumbar or sacral ple> a. Symptoms in the increased by movement, in the plexus itself a as in the arm. Wounds or contusions affecting the plexus, forcible retraction of the shoulder, gout, rheumatism, exposure and (in the new-born) obstetrical manipulations are the most common causes. i. Paralysis of deltoid, flexors of elbow, supina- tors and often the spinati. Pain and sensory loss in shoulder and outer side of arm. Neuritis in upper fart of plexus or, rarely, in J\fth and sixth cervical roots. ii. Paralysis in triceps, forearm muscles and hand muscles. Pain and sensory loss in liand, fore- arm and inner side of arm. Neuritis in lower part of plexus or, rarely, in seventh and eighth cervical and frst dorsal roots. b. Paralysis of flexors of hip, adductors of thigh and extensors of knee. Pain and sensory loss in lower part of abdomen, iront and sides of thigh and inner side of leg and foot. New growths in abdomen, caries of vertebra; and ascending infec- tion the common causes. Neuritis of lumbar plexus or roots. c. Paralysis of flexors and outward rotators of thigh, flexors of knee and muscles moving the foot and toes. Pain and sensory loss in back of thigh and all of leg and foot except inner side. Pelvic growths and inflammation, parturition and ascend- ing infection the common causes. Neuritis of sacral plexus. . Symptoms in the areas of a number of spinal nerves on both sides, especially the external popliteal and musculo-spiral nerves. Alcoholism is the most com- i 132 NERVOUS AND MENTAL DISEASES. mon cause ; other causes are pyemia, diphtheria and other infectious diseases, metallic poisons, exposure and ever-exertion. Multiple Neuritis. C. Onset of disease chronic (except very rarely in paral- ysis agitans when it follows a nervous shock) , but some symptoms, including paralysis, may come on rapidly, especially in disseminated sclerosis. 1 . Paralysis follows tremor which begins usually in one hand and gradually spreads. Voluntary motion is not entirely lost, but becomes more and more diffi- cult. The face becomes expressionless ; the head and shoulders are bent forward, the elbows, hips and knees are slightly flexed and the hands are held in the '' pill-rolling " position by a tonic spasm mainly affect- ing the flexor muscles (Fig. 20). The tremor usually persists during rest, but ceases temporarily during at- tempts to arrest it or to use the hand ; in rare cases it is entirely absent and the diagnosis must be made from the weakness and the characteristic posture. Tendon reflexes normal. No sensory loss or severe pain, but much distress and unrest. No positive signs of organic disease. Patient in second half of life. Paralysis Agitans, 2. There is intention tremor (well seen when the patient attempts to drink) which is generally associated with nystagmus, scanning speech or other signs of mul- tiple lesions. The paralysis may begin in individual muscles or in muscle groups, varying greatly in situ- ation in different cases. The affected muscles may waste and lose faradic irritability, but as a rule they do not. Tendon reflexes generally exaggerated. Be- gins during first half of life. Disseminated Sclerosis. 3. The paralysis is preceded by progressive dementia, often accompanied by delusions of grandeur, stum- bling speech, facial twitching and pupillary changes. A disease of middle life. Paretic Dementia. PARALYSIS OF PARTIAL OR IRREGULAR EXTENT. I33 4. Onset of paralysis always gradual and slow, in months or years. The paralyzed muscles slowly waste and lose faradic irritability. a. Atrophic paralysis begins in an adult patient, usually in the hand muscles, deltoid or upper arm muscles and after spreading more or less to others on the same side commonly attacks the other side in the same order. Fibrillation is common. Re- action of degeneration may occur in the cases of more rapid onset but not in the slower ones. The muscles are never enlarged and similar cases are very seldom found in the same family, i. There is loss of pain and temperature senses, often of greater extent than the atrophic pa- ralysis, with retention of touch sense in the same area. Other trophic changes such as glossy or thick and horny skin, whitlow, ulcera- tions, gangrene or degeneration of joints may occur. There may also be a spastic weakness of the legs without wasting. Syringomyelia . ii. There is no sensory loss and no other trophic symptom than muscular atrophy. § The atrophic paralysis in the upper part of the body is accompanied by spastic weak- ness of the legs without wasting. The tendon reflexes are exaggerated in both arms and legs. Amyotrophic Lateral Sclerosis. §§ Lower limbs not affected until late in the disease when their muscles are wasted and flabby. Tendon reflexes of the affected muscles diminished or lost. Spinal Muscular Atrophy, b. Atrophic paralysis begins in childhood in the dis- tribution of the peroneal nerves, causing talipes equinovarus. The disease slowly extends to the NERVOUS AND MENTAL DISEASES. muscles of the calves and thighs, and some years from the onset may involve the upper extremities (beginning in the intrinsic muscles of the hands) and the trunk. Fibrillation is common. Sensory Fm. ig. k (/'rom Goo/irs. loss may be observed. Other cases generally occur in the same family. Progressive Neural Muscular Atrophy. (Also called Peroneal Porm, Charcoi-Marie Type.) . Paralysis begins elsewhere than in hand muscles, PARALYSIS OF PARTIAL Oft IftftfiGULAft EXTENT. I35 deltoid or muscles supplied by the peroneal nerves. No fibrillation. No reaction of degeneration, gal- vanic and faradic irritability diminishing together. Other cases generally occur in the same family. Idiopathic Muscular Atrophy, i. Some of the weakened muscles are enlarged, usually the calves, infraspinati, quadriceps ex- tensors, glutei or lumbar muscles. Onset usu- ally in childhood (Fig. 19). Pseudo-hyper trophic Muscular Atrophy. ii. None of the weakened muscles is enlarged. Disease begins in childhood, youth or early adult life and usually first attacks the biceps, triceps, pectoral, latissimus, face, extensors of knee or flexors of hip. Simple Idiopathic Muscular Atrophy. 136 NERVOUS AND MENTAL DISEASES. ATAXIA. The patient is unable to stand or walk steadily, not on account of weakness alone, but because of incoordination of muscular action. There may also be disordered move- ment in the trunk and arms. I. A reeling gait and the associated symptoms, such as head- ache, vomiting, optic neuritis, paralysis in the domain of the cranial nerves or hemiplegia, indicate coarse intracranial disease directly or indirectly affecting the cerebellum or the region of the quadrigeminal bodies. The ataxia is not greatly increased by closing the eyes. A. Onset of symptoms sudden or very rapid, usually with loss or disturbance of consciousness. The arteries are atheromatous or syphilitic or there is endocarditis. No signs of suppuration. Hemorrhage^ Thrombosis or Embolism, B. Onset rapid or slow. There is a source of purulent in- fection, e.g,^ an infected wound of the scalp or cranium (especially compound fracture), otitis media, empyema or abscess in any part of the body. Rigors followed by fever and sweating common. Temperature irregular, mostly elevated but sometimes depressed. Duration may be short or it may be long with a period of latency. Optic neuritis is common but is rarely intense. Abscess, C. Onset chronic. No source of infection but a personal or family predisposition to new growths may be ap- parent. Temperature runs a normal or nearly normal course. Headache generally intense, often accompanied by vertigo and vomiting. Progressive mental failure occurs toward the end. Optic neuritis is the most char- ATAXIA, actenstic symptom ; it is present in foiir-fiiths of all cases and is usually intense. Course long and mostly progressive. Tumor. II. The associated symptoms, such as absence of knee-jerk, slight urinary difficulty, Argyll -Robertson pupil, optic atrophy, lightning pains, nystagmus, stumbling or scanning speech, or mental impairment of the paretic type, are of slow onset and indicate a degenerative disease affecting the spinal cord or both cord and brain. A. The ataxia of gait and station is greatly increased bv closing the eyes. The knee-jerks are absent except in rare cases in which advanced optic atrophy is an early symptom. A history of lightning pains in the legs is common, also of loss of virility, slight urinary difficulty and' ptosis or diplopia. Argyll-Robertson pupil in most cases. Tabes. B. A jerky or reeling gait begins in childhood or youth in members of certain predisposed fiimilies and is sooner or lajer accompanied by nystagmus, stumbling or blurred speech and incoordination of heck and arm muscles. Knee-jerks generally but not always absent, in rare cases increased. Paralysis and corresponding deformi- ties may occur, especially in the later stages. Hereditary Ataxia {^Friedreich's Disease). C. Weakness of legs and ataxia of gait and station begin in adult life and gradually increase. Knee-jerks and other tendon reflexes almost always increased, very rarely lost. Lightning pains very rare. Slight difficulty of articulation common. Ataxic Paraplegia. Xi. Intention tremor with nystagmus or scanning speech is associated with various signs of scattered lesions, such as isolated paralyses, contraction of the visual fields with impairment of color sense, loss of smelt, nervous deaf- ness, etc. Knee-jerks generally exaggerated. Disseminated sclerosis. Failure of judgment and memory, often combined with monstrous and unsystematized delusions of grandeuc. 138 NERVOUS AND MENTAL DISEASES. accompanies signs of organic disease, among which inequality of pupils, facial twitching and stumbling speech are common. Paretic Dementia, III. The associated symptoms (such as paralysis, wasting, loss . of faradic irritability, tenderness of muscles and nerves, numb stinging pain and some sensory loss, chiefly in the distribution of the external popliteal or external popfiteal and musculo-spiral nerves), together with evidence of a toxic in- fluence, indicate multiple neuritis. Knee-jerk lost except in the rarest cases. Argyll- Robertson pupil absent. Onset of ataxia usually acute or subacute, always more rapid than in the average case of tabes. Other symptoms may not be marked. A. History of prolonged alcoholic excess. Various signs of alcoholism may be present. Pain a prominent symp- tom. Alcoholic Neuritis. ^B. The ataxia is preceded by diphtheria. Onset of neuritis marked by loss of ocular accommodation and paralysis of the palate. Pain absent or slight. Diphtheritic Neuritis, C. History of acute or chronic poisoning by arsenic, or arsenic is found in the urine. Both arms and legs usually affected. Pain a prominent symptom. Herpes zoster common. Arsenical Neuritis, D. The ataxic form of neuritis may sometimes be due to various acute infectious diseases, malaria, septicemia, diabetes, beri-beri or leprosy. IV. There is no evidence of organic disease. The ataxia ap- pears first after an emotional disturbance and may increase or diminish in correspondence with emotional changes or sug- gestion. It may exist in any degree and sometimes pre- vents either standing or sitting (astasia-abasia) . Various signs of hysteria may be present. Hysterical Ataxia, TREMOR. 139 TREMOR. I. The tremor is due to emotion, exposure to cold or extreme fatigue in a healthy person. It is fine ; rate about 10 per second. Physiological Tremor, II. The tremor is an expression of the weakness of an exhaust- ing disease, such as typhoid fever, or of neurasthenia. It is fine and rapid and ceases during rest. Asthenic Tremor. III. The tremor is due to poisoning by alcohol, mercury, lead, arsenic, opium, chloral, tea, coffee or tobacco. Toxic Tremor, IV. The tremor is a symptom of organic disease of the nervous system, but is of slight diagnostic importance compared with other symptoms, as in hemiplegia, cerebral tumor or abscess, cerebellar disease, paretic dementia, tabes, hereditary ataxia, etc. Diagnosis as in Hemiplegia^ Optic Neuritis ^^ Head- ache^ Ataxia^ etc, V. Tremor is a prominent and important symptom. A. The tremor begins after forty years of age, usually in one hand, rarely in one leg and slowly extends to the other limb on the same side and then to the limbs on the opposite side. Its rate is five to seven oscillations a second and the range is generally small. As a rule it continues during rest and is lessened or stopped by effort ; rarely, in an early stage, it is elicited by effort. Following the tremor, beginning in the same part and spreading in the same order, muscular weakness and rigidity appear, the muscles, especially the flexors, grad- ually contracting so as to cause a characteristic posture with absence of facial expression. The hands assume the "pill-rolling" position; the knees, hips, wrists, elbows and shoulders, are somewhat flexed ; the head NERVOUS AND MENTAL DISEASES. and spine are bent forward (very rarely the head is bent backward) and the face stares straight ahead. Patients are restless, uncomfortable and unhappy and often com- plain of painful sensations of heat or cold. The tendon reflexes