Biomedical subjects
C M Fisher
Publications and source records attributed to C M Fisher.
Amnestic syndrome associated with propranolol toxicity: a case report.
An elderly woman developed an Alzheimer-like subacute dementia as a result of propranolol toxicity. Analysis of the manifestations showed that severe impairment of memory accounted for virtually all of the abnormalities. There is evidence that cerebral reactions to drug toxicity can exhibit patterns that suggest highly selective involvement of functional subdivisions of the brain.
Capsular infarcts: the underlying vascular lesions.
In ten patients, 11 infarcts involving mainly the internal capsule have been examined pathologically. Serial sections of the involved basal ganglia were studied in ten infarcts and only a gross dissection was made in the other. The implicated penetrating arteries were traced throughout their length and obstructive vascular lesions were found in nine instances. In two of the nine there was an atheromatous plaque with a superimposed thrombus, in four an atheromatous plaque had caused severe stenosis, in one a destructive arterial process lipohyalinosis had occurred, in one case the nature of the obstruction remained "uncertained," and in one the penetrating arteries were obstructed at their orifices by an atheroma in the superior division of the middle cerebral artery. In two cases the vessels were patent, suggesting embolism. The atheromas consisted almost exclusively of a conglomerate of fat-filled macrophages. The clinical correlate was a pure motor hemiplegia or hemiparesis involving the face, arm, and leg without sensory deficit, homonymous hemianopia, receptive aphasia, or apractognosia. Confusion was prominent in one patient.
Clinical and radiologic remission in reticulum cell sarcoma of the brain.
Two patients with cerebral reticulum cell sarcoma (CRCS) are reported in whom neurologic abnormalities and radiologic (computerized tomographic [CT] scan) evidence of tumor remitted. In one patient, remission followed craniectomy and corticosteroid therapy and lasted for eight months. In the other patient, at least four remissions occurred over a span of seven years, each in conjunction with the administration of corticosteroids. Corticosteroids may favorably alter the biologic activity of tumor tissue in some cases of CRCS, predisposing to clinical remission and disappearance of tumor on CT scan.
Symptomatic middle cerebral artery stenosis.
The clinical course of 16 consecutive patients with stenosis of the middle cerebral artery angiographically diagnosed between 1970 and 1977 was reviewed. All were managed nonsurgically with medical treatment including anticoagulation. Prior to therapy, transient ischemic attacks had occurred in 15 and cerebral infarction in 11. Initially, none exhibited more than a minor neurological deficit. Follow-up from one month to six years showed a benign course in 14 patients: 13 experienced no subsequent transient attacks or new stroke; 1 had repeated transient attacks for two years but not in the following four years. Two of the 16 developed a severe stroke early in the course, before medical therapy was started. No distinctive clinical or radiographic features were identified that permitted prediction of the outcome. This small series supports the need for a randomized study of bypass efficacy in these patients.
Syncope of obscure nature.
One hundred and eleven cases of syncope or loss of consciousness are analyzed. Most are of obscure nature while some illustrate features of syncope that deserve further scrutiny. The cases are divided into six groups: Resembling cardiac syncope (30 cases); vasovagal syncope (22 cases); features of both cardiac and vasovagal syncope (12 cases); orthostatic hypotensive (29 cases); akinetic seizure? (12 cases); and miscellaneous (5 cases). Some groups are subdivided according to the circumstances surrounding the spells, for example, seated eating, nocturnal, associated with bowel movement, response to anticonvulsant therapy, etc. The following conclusions seem warranted: The evidence favors the existence of a type of akinetic seizure resembling cardiac syncope; loss of consciousness while seated eating (prandial syncope) may comprise a syndrome; syncope related to bowel movement or abdominal pain is a striking association; sporadic nocturnal syncope due to temporary hyporeactivity of baroreceptors is not sufficiently recognized; alcohol ingestion may precipitate orthostatic hyporeactivity of baroreceptors is not sufficiently recognized; alcohol ingestion may precipitate orthostatic hypotension. Familial syncope, syncope proneness and cold drink syncope are illustrated.
Pyramidal infarction in the medulla: a cause of pure motor hemiplegia sparing the face.
We present a case with an infarct limited to the right pyramidal tract in the medulla. The lesion lay approximately 1 cm below the pontomedullary junction. On the basis of this case and three previously reported cases of medullary pyramidal infarction, there is defined a syndrome of severe hemiplegia with relative sparing of the face, tongue and articulation, minimal sensory loss, and good recovery. The hemiplegia is initially flaccid and later spastic. Transient symptoms, referable to the tegmentum of the medulla, occur at the onset, and reflect ischemia in the deeper territory of a paramedian penetrating vessel.
Reducing risks of cerebral embolism.
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Ataxic hemiparesis. A pathologic study.
Three stroke patients showed weakness and pyramidal signs on one side combined with a cerebellar-like ataxia on the same side. Pathologic study in each case showed an old infarct cavity in the basis pontis at the level of the junction of the upper one third and lower two thirds on the side opposite the neurologic deficit. The basilar artery was patent and the infarcts were probably the result of occlusion of penetrating arteries. This study demonstrates that a lesion of the basis pontis may be associated with a contralateral ataxia that is cerebellar in character. The designation ataxic hemiparesis is suggested for the syndrome.
Transient paralytic attacks of obscure nature: the question of non-convulsive seizure paralysis.
Eleven patients with transient paralytic attacks of obscure nature are described. Paralysis could involve face or leg alone, face and hand, or face, arm and leg. The duration varied from two minutes to one day. Four patients had brain tumors, six probably had brain infarcts, and one a degenerative process. The differential diagnosis included TIAs, migraine accompaniments, and seizures. In the absence of good evidence for the first two, the cases are discussed from the standpoint of possibly representing nonconvulsive seizure paralysis (ictal paralysis, inhibitory seizure paralysis or somatic inhibitory seizure). Because of the difficulty in defining seizures as well as TIAs and migraine in their atypical variations, a firm conclusion concerning the mechanisms of the spells was not attained. Two cases of the hypertensive amaurosis-seizure syndrome have been added as further examples of ictal deficits.
Thalamic pure sensory stroke: a pathologic study.
Two cases of pure sensory stroke were studied pathologically 6 months and 4 years after the acute illness. In both, there were lacunar infarcts in the region of the sensory nucleus of the thalamus on the side opposite the symptoms. The responsible vascular lesion in each case was hypertensive lipohyalinotic cerebral angiopathy, a process that correlates with the presence of hypertension. This was the first time that a complete clinicopathologic investigation was possible in pure sensory stroke and also the first time a lipohyalinotic lesion was shown to be the cause of a specific clinical syndrome.
Basal rupture of saccular aneurysm. A pathological case report.
In a case of subarachnoid hemorrhage, the arteries of the circle of Willis were left undisturbed and undissected at postmortem examination. A block of frontal lobe tissue with the attached vessels was serially sectioned disclosing in its entirety a saccular aneurysm that had ruptured at the base rather than the dome. The histology of the hemostatic process was clearly depicted.
Spontaneous dissection of cervico-cerebral arteries.
Sixteen cases of spontaneous dissection of the cervical internal carotid artery (6 verified) are described. The mean age was 45 years. The clinical picture varied from simply headache and a bruit to hemiplegia and aphasia. Eleven patients had transient ischemic attacks. Headache, facial pain, a subjective bruit, oculo-sympathetic palsy and transient monocular blindness were present in various combinations in two-thirds of cases and their presence suggested the correct diagnosis. Examples of suspected dissection of the intracranial internal carotid, middle cerebral, posterior cerebral and extracranial vertebral arteries are also presented. Spontaneous dissection is more common than the literature indicates.
Sensorimotor stroke due to thalamocapsular ischemia.
A 61-year-old hypertensive diabetic man awoke with a numb, heavy right arm and leg; symptoms progressed within 30 hours to a dense right hemisensory syndrome involving head, face, trunk, arm, and leg, accompanied by a right hemiparesis, involving tongue, face, arm, and leg with extensor plantar response, leaving him barely able to move the arm and leg against gravity. No impairment in alertness, memory, language, praxic, or visual functions was evident at any time. Improvement in motor function began in 24 hours and progressed to walking status by discharge on day 23. Eight days passed before the sensory deficit showed improvement, and it was still prominent at discharge. Autopsy three months later showed a 4 X 2 X 4-mm lacune in the ventral posterior nucleus of the left thalamus, with a zone of pallor on stained microscopic sections extending into the immediately adjacent posterior limb of the internal capsule. This case appears to be unique in that a sensorimotor stroke has been produced by a confirmed thalamocapsular infarct.
The human thalamocortical sensory path in the internal capsule: evidence from a small capsular hemorrhage causing a pure sensory stroke.
A patient is presented who suffered a strokelike event during life that resulted in a hemisensory dificit for some modalities. On pathological examination of the brain, the lesion responsible for the deficit was found to be a small slit hemorrhage located in the posterior limb of the internal capsule adjacent to and minimally involving the thalamus. Clinicopathological correlation suggests that the sensory thalamocortical radiations must lie farther posterior in the posterior limb of the internal capsule than the corticospinal motor fibers, and that they probably lie adjacent to the thalamus. The case emphasizes that small slit hemorrhages deep in the brain, although rare, must be considered in the differential diagnosis of sudden hemisensory deficits.
Influence of etiology of atrial fibrillation on incidence of systemic embolism.
Atrial fibrillation is well known to increase greatly the risk of systemic arterial embolism in patients with mitral valve disease. In light of the clinical frequency of embolism in patients with atrial fibrillation due to other types of heart disease, a study was made of embolic occurrences in 333 autopsy patients with atrial fibrillation associated with various kinds of heart disease. Considering only symptomatic emboli with pathologic or surgical confirmation, embolism occurred in 41% of patients with mitral valve disease, 35% of those with ischemic heart disease, 35% of those with coexisting mitral and ischemic heart disease and 17% of those with "other" types of heart disease. Embolism was found in only 7% of a control group of 58 autopsy patients with ischemic heart disease without atrial fibrillation. These findings suggest a high risk of embolism from atrial fibrillation of any origin, but particularly from that caused by ischemic heart disease and mitral valve disease.
Pure spastic paralysis of corticospinal origin.
This presentation includes six cases of chronic bilateral pure motor hemiplegia, one of these with pathological findings; one clinical case of chronic pure motor quadriplegia and one pathologically-studied case of chronic pure motor paraplegia. These cases may illustrate a spectrum of pure corticospinal disorders that heretofore has not been fully recognized.