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Biomedical subjects

C M Fisher

Publications and source records attributed to C M Fisher.

At least 91 records · Page 5Linked to original sources

Honored guest presentation: abulia minor vs. agitated behavior.

The neurological analysis of complex behavioral states associated with serious brain disease not infrequently is a difficult task. In many such cases, the signs of minor degrees of akinetic mutism were found when deliberately looked for. Recognition of this feature greatly facilitated interpretation. The ancient term abulia is suggested for the specific neurological syndrome comprising slowness, decreased responsiveness, apathy, etc. Akinetic mutism is its extreme form. A lesser degree of abulia is here termed abulia minor. The attributes of abulia minor are described, and the neurological conditions with which it had been found associated are listed. Preliminary conclusions as to the anatomical localization of the syndrome are presented. The literature on akinetic mutism is reviewed, and a few special observations are commented on--paradoxical activity, the telephone effect, and reflex attention. The application of the newer knowledge of cerebral neurotransmitters to akinetic mutism is illustrated. At the beginning of the study the focus was on abulia, but it was natural that sooner or later the contrasting state of behavioral hyperactivity or agitation would have to come under equal scrutiny. A list of conditions in which psychomotor agitation was a feature has been compiled from personal files. The localization of the disease process in hyperactive states is compared with that in abulia. A few special observations on hyperactive states are presented, along with a note on a unique syndrome termed anideation. There has gradually emerged a concept of a continuum of behavioral activity extending from abulia at one end through eukinesia to hyperactivity at the other end. Involvement of specific fundamental integrative circuits is postulated. This morning we have been enthralled by Computers in Neurosurgery, Neurobiology in Neurosurgery, and Humanism in Neurosurgery. What could be more natural for a neurologist than to talk about Neurology in Neurosurgery. And how best to pay homage to the great lady of Medicine than by offering a modest example of her handiwork. Thus, I am led to discuss a neurological theme which has recently occupied my attention. To anticipate a little, I shall be talking about two somewhat opposite states: on the one hand there is abulia--slowness, apathy, and lack of spontaneity--and on the other hand, agitation and hyperactivity. By way of explanation, this study originated during the bedside examination of patients with brain damage and serious impairment of analysis appeared not only formidable but even impossible.(ABSTRACT TRUNCATED AT 400 WORDS)

Akinetic Mutism↗

The relation of cerebral vasospasm to the extent and location of subarachnoid blood visualized by CT scan: a prospective study.

In 41 cases of verified ruptured saccular aneurysm, we prospectively predicted the presence or absence of delayed symptomatic cerebral vasospasm. CT criteria quantifying the extent and location of subarachnoid blood (developed in our previous retrospective study) were used in this prospective series of patients. Twenty-two patients had recognizable subarachnoid clots larger than 3 X 5 mm or layers of blood more than 1 mm thick (measured on reproduced images). In 20 of the 22 patients with severe significant clot or thick layer, severe vasospasm was correctly predicted and localized (2 false positives). In 19 patients with no blood, or diffuse blood, or blood outside the subarachnoid space, the absence of severe vasospasm was correctly predicted in 14 (5 false negatives). All of the false-positive and false-negative cases could be explained by inadequate CT technique. The data indicate that the extent and location of blood in the subarachnoid space determine the severity and location of vasospasm and that patients in jeopardy of developing symptomatic cerebral vasospasm can now be identified. Early preventive measures may now be assessed more accurately.

Adult↗

Disorientation for place.

The study of a patient with remarkable disorientation for place associated with an acute nondominant parietooccipital lesion raised the general question of a relationship between disorientation for place and topographical disorientation. The literature does not address this matter. The clinical findings of one case in particular are presented here in detail. Another six patients had been seen with a disproportionate disorientation for place; in each there was an acute insult to the nondominant hemisphere. Based on these cases, there is preliminary evidence of a possible relationship.

Adult↗

Transient global amnesia. Precipitating activities and other observations.

Impressed with the number of patients whose spells of transient global amnesia were triggered by special circumstances, I have reviewed 78 such cases. Precipitating events were reported in 26 of 85 spells: eight occurred during highly emotional experiences; seven, during sexual intercourse; six, while the patient was in pain; two, while a trigeminal ganglion was being stimulated; and three, during a dip in the cold Atlantic Ocean. These observations suggest an electrophysiologic disturbance. The characteristics of the amnesia, the organization of memory, and behavior during spells were also considered.

Aged↗

Neoplastic angioendotheliosis.

We add two cases of neoplastic angioendotheliosis to the previous 13 with central nervous system manifestations. This unusual neoplastic phenomenon is thought to represent a diffuse malignant proliferation of endothelial cells. A man aged 58 first had transient ischemic attacks followed by a subacute profound dementia with psychomotor retardation. Remission followed steroid therapy. Abulia recurred along with a gradually progressive paraplegia leading to death 16 months after onset of symptoms. Pathologic examination showed tumor masses in the basal ganglia and widespread patchy cerebral infarction. The spinal cord below the midthoracic level was destroyed. Microscopically small mononuclear tumor cells were widespread within and largely confined to the lumens of small cerebral blood vessels which showed varying degrees of occlusion and recanalization. Factor 8 antigen, a specific endothelial cell marker, was not present on the surface of the malignant cells. Another man aged 61 developed subacute dementia with frontal lobe signs, dysphasia and impairment of memory. Computerized tomography showed multiple infarcts. A brief respite followed steroid therapy but progressive deterioration led to death in 15 weeks. Frontal lobe biopsy revealed the same neoplastic vascular process. The hallmark of the illness is a progressive subacute lobar dementia. Transient spells may occur. Hemiparesis is unusual and seizures do not occur except terminally. Angiography is normal.

Arteries↗

Hydrocephalus as a cause of disturbances of gait in the elderly.

To investigate the possible role of symptomatic normal-pressure hydrocephalus (NPH) in unexplained walking difficulties of the elderly, we used CT to measure lateral ventricular size. We compared data in 50 patients over the age of 60 with a disturbance of gait and 80 control subjects of similar age who walked well and were mentally sound. Forty-six of the 50 gait patients (92%) had a ventricular span of more than 12 mm, whereas only 5 of the 80 controls (6.3%) had ventricles of that size. There was a narrow zone of overlap. Seventeen of the gait patients later improved after surgical shunting or test withdrawal of lumbar CSF. These findings demonstrate that hydrocephalus is an important cause of disturbances of walking in the elderly. The validity of the study, the clinical picture in NPH, and the nature of NPH are discussed.

Aged↗

Whiplash amnesia.

A 67-year-old woman was in the front seat of a stopped car that was struck from the rear by a truck. She was wearing a seat belt, and it was observed that her head did not strike the windshield. She immediately became amnesic and recovered in 72 hours. It is postulated that the transient amnesia was the result of a whiplash insult to the brain.

Accidents, Traffic↗

Lacunar strokes and infarcts: a review.

At least 20 different lacunar syndromes have been described and can be recognized by characteristic clinical features. Almost all occur in patients with hypertension. Small lacunes are usually due to lipohyalinosis, larger ones to atheromatous or embolic occlusion of a penetrating vessel. The concept of the "lacunar state" is examined in the light of recent knowledge with the conclusion that the clinical deficit is primarily related to unrecognized normal pressure hydrocephalus rather than to the presence of a few lacunes. The notion that lacunes occur haphazardly is criticized because the first or only lacune tends to be symptomatic. The incidence of cerebral lacunes has declined since the introduction of antihypertensive therapy, an indication that therapy is effective.

Aphasia↗

Cerebral atheromatous embolism following carotid sinus pressure.

Complications of carotid sinus pressure, which are rare, include cardiac arrhythmias and cerebrovascular accidents. A 79-year-old man experienced a flaccid right hemiplegia one minute after left carotid sinus pressure. At necropsy, an atheromatous embolus occluded the left middle cerebral artery, resulting in hemorrhagic infarction in its vascular territory. Atheromatous embolism following carotid sinus pressure has not been previously documented. Most sudden stroke deficits following carotid sinus pressure are probably caused by this mechanism.

Aged↗

Visual disturbances associated with quinidine and quinine.

Obscurations of vision were experienced by three patients taking quinidine and by two patients taking quinine. In four, transient symptoms developed on exposure to light after first awaking in the morning, and in the fifth, there was persistent photophobia. In two patients, there was a large central scotoma, in one, swirling dark clouds, and in the fourth, flickering of vision. The duration was 1 to 4 minutes in three patients and 45 to 60 minutes in one patient. The symptoms, which are benign, may be confused with the prodromal visual manifestations of thrombotic cerebrovascular disease.

Aged↗

Cholesterol embolism as a cause of transient ischemic attacks and cerebral infarction.

Although cerebral cholesterol embolism is a well-known process, the range of clinical manifestations has not been established. In the present case, the occurrence of transient ischemic attacks in association with cerebral cholesterol embolism is described for the first time. A 69-year-old man experienced multiple 5- to 8-minute spells of numbness or weakness involving one or the other hand in 3 years. The attacks continued despite warfarin therapy. When the left arm became permanently paralyzed, an ulcerative plaque was removed from the right internal carotid artery, but the neurologic deficits increased. Progressive renal failure developed, and he died 5 months after the initial medical evaluation. Neuropathologic examination disclosed multiple small infarcts in both cerebral hemispheres, predominantly in the border-zone territory on the right side. Many small cerebral arteries were occluded by cholesterol emboli. Anticoagulant therapy appeared to exert an adverse affect.

Aged↗

Oval pupils.

The records of 17 patients whose neurological examination disclosed oval pupils in one or both eyes were reviewed. Sixteen of the 17 had serious cerebrovascular illnesses--hypertensive cerebral hemorrhage (five patients), ruptured saccular aneurysm (five patients), epidural hemorrhage (one patient), bilateral cerebral infarction (two patients), brainstem strokes (two patients), and cerebral anoxia (one patient). One patient was recovering from an oculomotor palsy. Oval pupils usually represent a transient, unstable phase in progressive injury to the oculomotor complex and less frequently a transient phase of recovery.

Aged↗

Relation of cerebral vasospasm to subarachnoid hemorrhage visualized by computerized tomographic scanning.

In 47 cases of verified ruptured saccular aneurysm, we investigated the relationship of the amount and distribution of subarachnoid blood detected by computerized tomography to the later development of cerebral vasospasm. When the subarachnoid blood was not detected or was distributed diffusely, severe vasospasm was almost never encounters (1 of 18 cases). In the presence of subarachnoid blood clots larger than 5 X 3 mm (measured on the reproduced images) or layers of blood 1 mm or more thick in fissures and vertical cisterns, severe spasm followed almost invariably (23 of 24 cases). There was an almost exact correspondence between the site of the major subarachnoid blood clots and the location of severe vasospasm. Every patient with severe vasospasm manifested delayed symptoms and signs. Excellent correlation existed between the particular artery in vasospasm and the delayed clinical syndrome. Severe vasospasm involved the anterior cerebral artery in 20 cases and the middle cerebral artery in only 14. As the grading system used is partly subjective, the findings should be regarded as preliminary. The results, if confirmed, indicate that blood localized in the subarachnoid space in sufficient amount at specific sites is the only important etiological factor in vasospasm. It should be possible to identify patients in jeopardy from vasospasm and institute early preventive measures. (Neurosurgery, 6: 1--9, 1980)

Adult↗

Late-life migraine accompaniments as a cause of unexplained transient ischemic attacks.

Occasionally patients in the stroke age-bracket over 40 have unexplained transient cerebral ischemic attacks in association with normal cerebral angiograms. From this group 120 have been collected in whom the transient episodes resembled the neurological accompaniments of migraine. According to symptoms, the patients were categorized as follows: Visual accompaniments (patients with only ordinary scintillating scotoma were excluded), 25; visual and paresthesias, 18; visual and speech disturbance, 7; visual, and brain stem symptoms, 14; visual, paresthesias, and speech disturbance, 7; visual, paresthesias, speech disturbance and paresis, 25; recurrence of old stroke deficit, 9; miscellaneous, 8. In establishing the diagnosis angiography is advisable in all but classical cases. Typical of migrainous accompaniments are the buildup and migration of visual scintillations, the march of paresthesiae, and progression from one accompaniment to another, characteristics that do not occur in thrombosis and embolism. Diagnosis facilitated when 2 or more similar episodes have occurred or migraine-like scintillations are present. Headache occurred in 50% of cases. Other cerebrovascular processes, coagulation disorders, and cerebral seizures must be ruled out.

Adult↗

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.

Aged↗