Complete Text (Part 8)

course of a few weeks. Choreic Paralysis, B. Onset variable; if sudden it may suggest apoplexy, especially when it occurs in an hysterical fit ; if gradual the paralysis may advance in steps from one joint to the next. An emotional cause is often distinctly apparent. Sus- ceptibility to suggestion is apparent in the history or at the examination. History of hysterical attacks common. Hysterogenic zones may perhaps be found. Symptoms often vary greatly with emotional changes. When the patient is urged to attempt a movement the opposing muscles may often be seen to resist it. If at- tention be diverted acts requiring the use of the paralyzed 98 NERVOUS AND MENTAL DISEASES. muscles may perhaps be performed automatically. Under encouragement, especially if electricity or other local treatment has been used, a far greater movement may be made than at first seemed possible. When the leg is involved and the patient walks, the toes do not, as in organic paralysis, keep to the ground from the mere weight of the foot, necessitating an exaggerated motion of the hip by which the lame foot is swung in advance of the sound one ; on the contrary, the foot is often held in a fixed position and is usually dragged after the sound one instead of advancing before it. Sensory loss is often more extensive and profound than the paralysis and its distribution is characteristic of hysteria, being most commonly in the form of hemi- anesthesia with corresponding impairment of the special senses, or in areas bounded by the external lines of the body or by circular lines around a limb, or in geometric areas, but never corresponding exactly to the distribu- tion of particular nerves or spinal segments. Hysterical Paralysis. LOCALIZATION DIAGNOSIS. 99 LOCALIZATION DIAGNOSIS IN PARTIAL HEMIPLEGIA AND MONOPLEGIA. For most cases the seat of the lesion has already been sufficiently indicated. In cases of spastic partial hemi- plegia or monoplegia of intracranial origin, localization depends on the same principles as in hemiplegia (which see), but the lesion is almost always in the cortex or cen- trum ovale, because there the motor tract is so spread out as to admit of the fibers for the face, arm or leg, being damaged separately ; in the internal capsule, crus or pons, these fibers are so close together that a lesion of any con- siderable size must affect all of them and so cause a com- plete hemiplegia. lOO NERVOUS AND MENTAL DISEASES. PARAPLEGIA— DOUBLE HEMIPLEGIA. Both legs are paralyzed, with or without paralysis of the arms and face. I. Organic disease of the nervous system is shown to be pres- ent by some positive sign, e, g.^ paralysis and sensory loss corresponding definitely to the distribution of nerves or the function of spinal segments, angular deformity of spine, girdle sensation or other root symptoms, degenerative atrophy of muscles, loss of faradic irritability, absence of knee-jerk, typical ankle clonus, paralysis of face, tongue, ocular muscles or one side of larynx, optic neuritis or atrophy, absence of light reaction, etc. A. There is no paralysis, spasm or sensory loss, except in parts innervated by the spinal cord and in such form as to be accounted for by disease of the cord itself. I . There is more or less sensory loss in addition to the paralysis, the upper limit of both corresponding to a segment of the spinal cord, generally combined with disturbed action of the bladder and rectum. Not preceded by localized spinal pain and rigidity. a. Onset sudden in a few moments. i. Simultaneous with severe injury to spinal column. JRracture or Dislocation of Vertebrce^ Wound of or Hemorrhage into Cord. ii. Without external violence. Hemorrhage into Cord. b. Onset gradual, acute or chronic. Vertebrae not diseased. Pain rarely a prominent symptom, al- though some dull pain is usually present. Myelitis. PARAPLEGIA DOUBLE HEMIPLEGIA. Paralysis preceded by localized spinal pain nnJ rigid- ity; corresponding radiating pains common. Paral- ysis of legs spastic with exaggeration of knee- and Achilles- jerks, unless the disease be low enough to involve the lumbar enlargement, in which case wast- ing and loss of tendon reflexes will be found. Sen- sory loss and disturbance of bladder and rectum may or may not be added to th',- other symptoms. a. Deformity or swelli.ig, often with deep-seated tenderness, indicates disease of the vertebric. i. Patient most commonly a child, sometimes an adult, rarely an elderly person. The tubercular diathesis is almost always mani- fest, but very rarely syphilis may be the cause. The pain, generally of moderate severity, is increased by motion or jars and diminished by rest of spine. Prominence or lateral displacement of one or more spinous processes the characteristic deformity. Spinal Caries. ii. Patient generally in second half of life. There may be a history of tumor elsewhere or of predisposition to new growths or to aneurism. Pain very intense and greatly aggravated by motion. § Radiating pain mainly in the a dorsal segments. seat of deformity. Aneurism eroding Spine. SS Fain on both sides. No thrill or mur- mur. Tumor of Spine, Nothing to indicate disease of vertebra, i. Onset sudden or rapid after passing from an air pressure of three atmospheres or more to the ordinary pressure. Headache, giddiness, abdominal pains and vomiting common. CoissoTi Dls left side of thorax, of the fifth and sixth Thrill and i I02 NERVOUS AND MENTAL DISEASES. ii. Onset sudden. No fever at first. Spinal Meningeal Hemorrhage, iii. Onset gradual but rapid, marked by chill and fever. Acute Spinal Meningitis, iv. Onset gradual and slow. § History of alcoholism, syphilis or ex- posure to cold. Chronic Spinal Meningitis. § § Evidence of predisposition to new growths. No other cause of meningitis. Intraspinal Tumor, B. Symptoms in parts innervated by the spinal cord greatly predominate over such cerebral or cranial nerve symp- toms as may occur and often exist alone. No localized spinal pain, rigidity or radiating pains. I. Paralysis always flabby with loss of tendon reflexes. Onset acute or subacute. a. Onset in a few hours to a few days and resembles that of an eruptive fever ; often marked by vomit- ing, sometimes by convulsions ; attended by rheu- matoid pains. Paralysis is usually unequal on the two sides and is rapidly followed by wasting and loss of faradic irritability. Anterior tibial group and peronei generally most affected. No disturb- ance of bladder or rectum. No sensory loss. Six- sevenths of all cases occur in children under ten years of age. Poliomyelitis. b. Onset acute. Paralysis begins in legs and ascends rapidly through trunk to arms. No wasting or change in electrical reactions. No severe pain. There may be slight and ill-defined sensory loss and perhaps disturbance of bladder and rectum. Fever generally absent. Most cases occur in early adult life during convalescence from some acute infectious disease or after exposure to cold. Acute Ascending Paralysis. c. Onset acute or subacute, in one to four weeks or PARAPLEGIA DOUBLE HEMIPLEGIA. IO3 more. Paralysis, niiiiib, stinging pain and more or less sensory loss are in the distribution of pe- ripheral nerve trunks, especially the external pop- liteal and musculo-spiral. Muscles and ner'es tender. Bladder and rectum verj- rarely invoK'ed. Usually a history of alcoholism, metallic poison- ing, diphtheria, septicemia, extraordinary exer- tion or exposure to cold. Multiple Neuritis. 3. Paralysis spastic with exaggeration of tendon re- flexes. Onset of disease always slow, although in disseminated sclerosis paralysis and other symptoms may come on rapidly. Bladder and rectum not affected until disease is far advanced. a. Paralysis is accompanied by intention tremor, nvstagmus, scanning speech or other signs of scattered lesions. Disseminated Sclerosis. b. No evidence of disseminated sclerosis. No sen- sory loss. i. The spastic paraplegia is accompanied by de- generative muscular atrophy and fibrillary twitching in the upper part of the body, gen- erally beginning in the liand, shoulder or back. Amyotrophic Lateral Sclerosis. ii. Paraplegia accompanied bv ataxia. Postero-lateral Sclerosis. iii. Paraplegia without muscular atrophy or ataxia. Lateral Sclerosis. C. Cerebral symptoms predominate over any signs of spinal disease that may accompany them. I. Onset acute, marked by intense headache and fever. Delirium occurs early and is often followed by sopor and coma. Retraction of head occurs in almost all cases. Spinal rigidity and pain, both localized and radiating, together with cranial nerve symptoms, common. An eruption of herpes, purpura, urticaria or erythema occurs in most cases. No apparent except epidemic inllueace. Whole course I04 NERVOUS AND MENTAL DISEASES. from onset to fatal ending or established convales- cence varies from a few hours to a few months. Cerebrospinal Meningitis. 2. Onset of disease chronic. The paraplegia is either spastic or ataxic and may be of slow or rapid onset. Progressive mental failure (often with delusions of grandeur), inequality of pupils, stumbling speech and slight facial twitching are the most characteristic symptoms. Paretic Dementia, 3. Onset usually sudden or very rapid, occurring in most cases at birth or in infancy, but it may be slow and occur at any age. No conclusive sign of spinal disease but cerebral symptoms (disturbance of con- sciousness, mental defect, aphasia, convulsions, etc.) and cranial nerve symptoms are common. Paralysis spastic with exaggeration of tendon reflexes except for a short time immediately after a sudden onset. Control of bladder and rectum sometimes impaired and involuntary evacuations may also occur through inattention. Bilateral Lesion of Hemispheres or^ possibly^ a single one of Pons ^ kind of lesion determined as in Hemiplegia^ q, v. II. All positive signs of organic disease absent, although an atypical ankle clonus may be found, especially in cases of long standing with contracture of the calf muscles. A. Onset variable. An emotional cause is often apparent. Susceptibility to suggestion is generally manifest in the history or at the examination. History of hysterical at- tacks common ; hysterogenic zones may perhaps be found. Symptoms often vary greatly with emotional changes. When the patient is urged to attempt a move- ment the opposing muscles may often be seen to resist it. If attention be diverted movements of the paralyzed limbs sometimes occur automatically and under encour- agement, especially if electricity or other local treatment has been used, a far greater movement may be made DllOKAM V>OM Th« cndi of the vertebral »plne» are opposite the iat4A\« ol ttuii ot>ti "ik««* oAh "» He lumbar rejion. They correspond to Vat \iniBt eftije ot ttitVi (m*^*****"-** eerrialaad lut two dortal, and to the uppei part o( Wit VA^^xiW"^''^-'*" Uie (tonal r«g^oD. I06 NERVOUS AND MENTAL DISEASES. than at first seemed possible. Sensory loss is common, never corresponding to the distribution of particular nerves or spinal segments, but in areas bounded by the external lines of the body or by circular lines around a limb, or in geometric areas. Hysterical Paraplegia, B. Paraplegia does not appear when the patient is lying down but only on attempting to walk or stand or, rarely, while sitting. The affection is usually hysterical but not always certainly so. Astasia Abasia. LOCALIZATION DIAGNOSIS. LOCALIZATION DIAGNOSIS IN PARAPLEGIA AND DOUBLE HEMIPLEGIA. S final Localization. — The spinal cord is hypothetically divided into segments, each one being numbered like the pair of nerves connected with it; thus we have eight cerv- ical, twelve dorsal (or thoracic), five lumbar and five sacral segments. Each of these segments is higher than its cor- responding vertebra ; the relation of segments, nerve roots and verlebrje to each other is shown in the accompanying diagram from Gowers. The upper limit of a coarse spinal lesion may be deter- mined in three ways : 1, By comparing the upper limit of the sensory loss with the sensory areas supplied by the several spinal seg- ments as given in Figs. 28 and 29 ; sometimes the limit of anesthesia is made especially distinct by a zone of hyperes- thesia immediately above it. 2, By comparing the upward Hmit of the paralysis and loss of faradic irritability with the table on the next page showing the relation of muscles to spinal segments. 3, By comparing the loss of reflexes with the part of the same table showing the relation of reflexes to spinal seg- ments. In determining the lower limit of the lesion it is obvious that sensory loss and paralysis cannot be utilized but the good condition of segments below the lesion will usually he indicated by the absence of atrophy, the presence of faradic irritability and the reflex response of the corre- sponding muscles. For example, in a case of gunshot Table Modified from Gowers, 'Showing the Approxi- MATE Relation of Spinal Segments to Muscles and Reflexes. Muscles. Segments. Muscles. Segments. C I ) Small rotators of head. C i Reflexes. Stern o mastoid. Upper neck muscles. Upper part of Trapezius. Lower neck muscles. I Middle part of Trapezius. Shoulder. Muscles. D.} 2 J Depressors of hyoid. 3 Lev. ang. scapulae. > Diaphragm. 5 J Serratus. . Flexors of elbow. Supinators. Extensors of wrist and fingers. 7 ^ Ext. elbow. >■ Flex, wrist and fingers, oj Pronators. 2 3 4 } Biceps-jerk. Triceps-jerk. Wrist-j. (ext.) Wrist-j.(fiex.) Intrinsic muscles of hand. D i Palmar. Lower part of Trapezius and Dorsal muscles. ► Intercostals. Lumbar muscles. Peronei. Flex, of ankle. Ext. of ankle. 2 3 4 5 6 7 8 9 ID' II 12 L I 2 ^ Cremaster. Epigastric. ►Abdominal muscles. \ 3I Flexors of hip. Extensors of knee. I Adductors of hip. Abdominal. Cremasteric. Knee-jerk. ] } ) 1 Ext. and abductors of hip. Flexors of knee. Intrinsic muscles of foot. 4 5 S iJ t 4 5 Co. Perineal and anal muscles. 4 5 Co. Gluteal. Heel-jerk. Plantar. Perineal, anal and vesical. c/5 LOCALIZATION DIAGNOSIS. IO9 wound of the cord there was sensory loss up to the line between the first and second himbar areas; there was paralysis of all joints of both lower limbs with correspond- ing loss of faradic irritability and reflexes. This indicated an extensive lesion in the lumbar enlargement and that the second lumbar was the uppermost segment involved. But the anal and perineal reflexes were lively and the faradic irritability of the perineal muscles was retained : there was complete retention of urine until a large quantity- had accumulated and then there was a purely reflex evacu- ation. This indicated that the lower sacra) segments were not involved. Consulting Fig. i6 it will be seen that the damaged portion of the cord, extending from the second lumbar to the second sacral segment inclusive, was con- tained mainly by the twelfth dorsal vertebra, not extend- ing as high as the upper border of the eleventh or as low as the lower border of the first lumbar. An operation was performed and the bullet found within the spinal canal just ■ above the lower border of the eleventh dorsal vertebra. Cerebral Localization. — The cerebral lesions that cause double hemiplegia or paraplegia act in precisely the same way as those which cause hemiplegia, the only difference being that both sides of the brain are affected in.stead of one, and they are localized by applying the same princi- ples as in hemiplegia. The history of the onset nnust be carefully studied. If paralysis has occurred in two distinct attacks, first on one side and then on the other, the symptoms attributable to each must be considered separately, for in such a case there are two lesions, having no connection except that of a common cause, such as syphilis or arteriosclerosis. Assuming that a single lesion has caused paralysis both sides, the localizing symptoms may be arranged iollows : =J no NERVOUS AND MENTAL DISEASES. LOCALIZATION DIAGNOSIS IN DOUBLE HEMI- PLEGIA OR PARAPLEGIA OF INTRA- CRANIAL ORIGIN. I. Spastic paralysis of both legs, perhaps also involving the arms but to a lesser degree, has its onset at birth or in in- fancy. Epilepsy, delayed acquisition of speech or intellec- tual defects almost invariably present. Cerebral Birth Palsy or Infantile Cerebral Palsy ^ due to bilateral meningeal hemorrhage or cortical throm- bosis, II. Spastic paralysis of both legs occurs along vv^ith symptoms indicating an intracranial tumor. Growth near the Vertex^ pressing on both paracentral lobules, III. There is double hemiplegia along vv^ith paralysis of the third or fourth nerve on either side. Hemianopia may be pres- ent. Optic neuritis and other signs of a tumor likely to be present. Lesion of both Crura, IV. Double hemiplegia is accompanied by paralysis of the seventh, sixth or motor branch of the fifth nerve, on either side, or by anesthesia of the face. Sw^allowing and articu- lation generally impaired. Hyperpyrexia and a rapidly fatal course common in acute lesions. Bilateral lesion of Pons, V. Paralysis on both sides of the body (perhaps irregularly dis- tributed) is accompanied by paralysis of the lips, tongue, palate, pharynx and larynx. Acute lesions rapidly fatal. (See Bulbar Paralysis.) Lesion of the Medulla, PARALYSIS OF OCULAR MUSCLES, PARALYSIS OF OCULAR MUSCLES. I. The paralysis is not limited to the associated movements of both eyes which can be made voluntarily by normal indi- viduals, such as convergence or conjugate movement to the right or left, but when the eyes are tested separately a motion which is not separatelv under the control of the will is found to be lost on one side independently of the action of the other. Paralysis of the levator is revealed by ptosis ; of the external muscles of the eve-ball by limitation of move- ment in the direction of the affected muscle, secondary deviation of the sound eve and diplopia ; of the internal ocular muscles by the absence of accommodation or of pupillary action. Spasm simulating ptosis, spasmodic stra- bismus or spasm of the muscle of accommodation must not I be mistaken for paralysis. A. The paralysis is caused by hemorrhage, inrtanimiition or new growth within the orbit. B. The paralysis is not caused by disease within the orbit. I, The paralysis is congenital, often associated with Error of Development of nuclei^ nerve trunks or muscles. , The