Loss of the ability to write from dictation. Preservation of the power of writing spontaneously. 5. Transcortical sensory aphasia (Fig. 16, 5). Loss of the power of comprehending speech. Loss of the power of comprehending writing. Preservation of the power of spontaneous speech, with paraphasia. Preservation of the power of repeating words, without ability to comprehend them. Preservation of the ability to read aloud, without the power of comprehending words. Preservation of the ability to write spontaneously, with paragraphia. Preservation of the ability to write from dictation without the power of comprehension. Preservation of the ability to write by transcript. 6. Subcortical sensory aphasia (Fig. 16, 6). Loss of the power of comprehending speech. Loss of the power of repeating words. Loss of the ability to write from dictation. Preservation of the power of comprehending writing. 7. Conduction-aphasia (Fig. 16, 7). Loss of the power of repeating words. Loss of the ability to read aloud. Loss of the ability to write from dictation. Preservation of the power of spontaneous speech, with par aphasia. Preservation of the power of comprehending writing. Preservation of the power of comprehending speech. Preservation of the power of writing spontaneously, with par agraphia. Preservation of the ability to write by transcript. Most commonly aphasia occurs in association with right-sided cerebral hemiplegia. This is to be attributed to the fact that emboli and thrombi, the most common causes of aphasia, are, as a rule, situated in the middle cerebral artery or the artery of the fossa of Sylvius, so that, in addition to the third frontal and the first temporal convolution, also the two central convolutions, with their motor cortical centers, are deprived of their blood-supply (p. 42, Fig. 13). Aphasia without motor paralysis and pure varieties of aphasia occur only in association with the presence of small circumscribed lesions, as, for instance, tumors, abscesses, localized meningitis, and injuries. Thus, an observation is on record in which a man, after having been thrown from a horse, became suddenly aphasic, because a splinter, sprung from the vitreous plate of one of the cranial bones, lacerated the left third frontal convolution in Broca's area. At times aphasic manifestations occur so abruptly as a transitory manifestation that circulatory disturbances in the speech-convolutions susceptible of being compensated for must be thought of. Such manifestations have been observed in cases of hysteria, epilepsy, uremia, and after infectious diseases and intoxications. Aphasia will disappear also, although more slowly, if it be not the result of a lesion of the speech-cortex, but is a remote symptom in the presence of hemorrhage, neoplasm, abscess, or an inflammatory process in the neighborhood of the speech-convolutions, and the pressure or analogous disturbance subside with the occurrence and the progress of absorption. Congenital aphasia has occasionally been observed. It is noteworthy that in a case of aphasia the brain may appear normal to the unaided eye, and only on microscopic examination will the changes in the cerebral cortex be disclosed. Aphasic disturbances are susceptible of improvement, and occasionally of cure. These ends may be attained by speech-exercises. Patients suffering from motor aphasia should be made to repeat words, passing from the simple to the complex, and constantly repeating the same words until they are retained. Patients with amnesic aphasia are best educated by means of pictures. Naturally, much patience will be required on the part of both pupil and teacher. Care should be taken not to tire the patient, as aphasic individuals readily become impatient and angry. The greatest difficulty is encountered in the treatment of total aphasiathat is, simultaneous motor and sensory aphasia-as the means of communication with the patient are so limited. The possibility of learning to speak depends upon whether some parts of the speech-centers still persist, or whether the corresponding portions of the right cerebral hemisphere can be trained in the faculty of speech. Naturally, the primary disorder should be treated in accordance with the usual rules. CEREBRAL ANEMIA. Etiology. Although the brain responds most delicately in function to all circulatory alterations, cerebral anemia but rarely acquires independent clinical significance. Cerebral anemia may, naturally, occur after profuse loss of blood, whether this takes place following injury or operation, or from the nose, the stomach, the intestine, the uterus, and the like. A deficiency in the hemoglobin of the blood exerts the same effect as hemorrhage, and symptoms of cerebral anemia are therefore observed in association with chlorosis, leukemia, pseudoleukemia, progressive pernicious anemia, the carcinomatous cachexia, long-continued diarrhea, and purulent and other wasting discharges. Cerebral anemia occurs not rarely in consequence of spasm of the cerebral arteries. Such an occurrence may be induced by an offensive visual impression, and even by a harrowing recital, by fright or pain, and then frequently causes fainting-syncope. Occasionally cerebral anemia is induced by the sudden diversion of an excessive amount of blood to other organs. Thus, it is observed at times after too rapid evacuation of peritoneal or pleural effusions. Also, the manifestations of shock following general concussion and traumatism are to be explained by paralysis of the splanchnic nerve, in consequence of which the blood-vessels of the abdominal viscera become greatly dilated and excessively filled with blood, while the brain is correspondingly deprived of blood. At times symptoms of cerebral anemia appear after a copious evacuation from the bowels that has for a long time been preceded by constipation, because the intestinal blood-vessels, previously compressed by the fecal accumulation, suddenly receive large amounts of blood after the expulsion of the contents of the bowel. Cerebral anemia may result from cardiac weakness, and is observed especially in conjunction with fat heart, because the heart is unable to propel a sufficient amount of blood into the brain. The disturbances generally occur in the upright posture. Symptoms of cerebral anemia appear not rarely also in association with stenosis of the aortic orifice. Cerebral anemia may develop in consequence of increased cerebral pressure, induced either from within outward (internal hydrocephalus) or being exerted from without inward (diffuse meningitis). Circumscribed cerebral anemia, such as occurs in connection with neoplasms, abscesses, hemorrhage, embolism and thrombosis of the cerebral arteries, may for the present be omitted from consideration. Anatomic Alterations. In the presence of cerebral anemia the brain-tissue is characterized by unusual pallor. Often the boundary between the white and the gray matter is ill defined. The brain-tissue is rather firm, providing that cerebral edema is not present together with cerebral anemia. The meninges also appear anemic, and this may be readily comprehended from the fact that they transmit the blood-vessels to the brain. The cerebral sinuses contain a small amount of blood and sometimes none. Symptoms and Diagnosis. In accordance with the mode of development and the course of the disorder a distinction is made between acute, subacute, and chronic cerebral anemia. The most acute form of cerebral anemia is probably that which develops in consequence of vascular spasm. Under such conditions there generally occurs a sense of oppression in the precordium, and often also palpitation of the heart. The face becomes pale; the patient manifests a tendency to yawn; nausea is present, and occasionally vomiting takes place. The extremities become heavy and the skin rough; ringing in the ears occurs, with spots before the eyes, and then obscuration of the field of vision and loss of the sense of hearing. The pupils become contracted, and finally the patient falls, with loss of consciousness, often with a slight cry, and general clonic muscular contractions. The duration of the loss of consciousness or fainting-syncope-varies from a few seconds to a few minutes. Restoration to consciousness occurs with varying rapidity. Cerebral anemia due to hemorrhage gives rise to quite the same manifestations, except that these develop rather more slowly and in somewhat of a subacute manner. Chronic discharges are followed by the clinical picture of chronic cerebral anemia, consisting in part of irritative and in part of paralytic phenomena referable to the brain. The patients complain frequently of vertigo, headache, sleeplessness (agrypnia), ringing in the ears, spots before the eyes, and palpitation of the heart, and they not rarely exhibit delirium (of inanition). Often complaint is made of paresthesia in the lower extremities, and occasionally also of clonic muscular contractions and paresis. All of the symptoms are increased in the upright posture and may be followed by obscuration of the visual field, general clonic muscular spasm, loss of consciousness, and even death. The recognition of cerebral anemia is easy; the appearance of the patient and the etiology will suggest the diagnosis. Prognosis. The prognosis of cerebral anemia is favorable if the causative factors are curable and the condition of general anemia is not excessive. Treatment. In the presence of cerebral anemia it is always important to place the patient in the horizontal posture, with the head dependent. In other respects the treatment varies with the causative factors operative in the individual case-causal therapy. In the presence of vasomotor spasm due to fright stimulating remedies should be employed, as, for instance, application with friction to the forehead of cologne-water or vinegar, inhalation of ammonia, irritation of the nose with a feather, tickling or brushing the sole of the foot, subcutaneous injections of camphorated oil, from 5 to 10 drops of sulphuric ether internally, and the like. When the loss of blood has been large the extremities should be bandaged in order to force the blood into the internal viscera, and transfusion or infusion of physiologic salt-solution should be praetised. When the amount of hemoglobin is deficient preparations of iron will be indicated, and when wasting discharges have taken place a nutritious diet. 4-II. CEREBRAL HYPEREMIA. Etiology.-Extremely little of a definite nature is known with regard to the clinical significance of cerebral hyperemia. At any rate, but subordinate importance can as yet be attached to it. In the first place, a distinction must be made between arterial and venous hyperemia of the brain, accordingly as the condition is dependent upon an abnormal increase in the supply of arterial blood or upon interference with the escape of venous blood. Arterial hyperemia of the brain has also been designated congestive or active, and venous hyperemia, passive or hypostatic. Arterial hyperemia of the brain may result from increased activity on the part of the heart-muscle, such as occurs transiently following psychic and physical exertion, after a heavy meal and the use of large amounts of alcohol, and persistently in the presence of hypertrophy of the left ventricle of the heart from any cause (aortic valvular insufficiency, arteriosclerosis, contracted kidney, idiopathic hypertrophy of the heart). At times cerebral hyperemia develops because the supply of arterial blood to certain portions of the body is interfered with. Such a condition is observed in association with abdominal tumors, ascites, peritonitis, constipation, and aortic stenosis. Cerebral hyperemia may result also from paralysis of the vasomotor nerve, which arises from the cervical sympathetic. Thus, a number of poisons (alcohol, amyl nitrite, nitroglycerin) are capable of causing paralytic arterial hyperemia of the brain. The most common variety of renous hyperemia of the brain depends upon conditions of weakness involving the muscular wall of the right side of the heart, which render impossible complete emptying of the right ventricle with the systole, so that bloodstasis extends from this cavity to the right auricle, thence to both venæ cavæ, and from the superior vena cava also to the internal jugular veins, the sinuses of the dura mater, and the cerebral veins. Such conditions develop with especial frequency in the presence of valvular lesions of the heart and diseases of the myocardium, the pericardium, and the respiratory organs (pulmonary emphysema, chronic bronchial catarrh, extensive pleural adhesions). At times venous hyperemia of the brain results from pressure upon the superior vena cava or its peripheral branches, such as may readily occur in the presence of an aortic aneurysm, a mediastinal tumor, an enlarged thyroid gland, and enlargement of the cervical lymphatic glands. Thrombosis of the internal jugular veins or of the cerebral sinuses should also be mentioned among the causes of hypostatic hyperemia of the brain. It should not be overlooked that expulsive efforts may give rise to blood-stasis. Therefore, those who engage in the act of blowing, who suffer from cough and from constipation, and who are engaged in arduous pursuits |