Cell loss and shrinkage in the nucleus basalis Meynert complex in Alzheimer's disease.

Marked neuron loss in the nucleus basalis of Meynert complex (NBMC) in Alzheimer's disease has repeatedly been reported in the literature. However, most of these studies quantitated only magnocellular, hyperchromatic (putative cholinergic) neurons of just a small part of the NBMC, and counts were expressed as numerical density. Applying a 3-dimensional-sampling design throughout the entire rostrocaudal extent of the NBMC and sampling neurons regardless of their size and staining characteristics, an overall neuron loss of only 15.5% was demonstrated for the whole NBMC. Neuron loss varied from 0% rostrally in the NBMC up to 36% in the most caudal part of the nucleus basalis of Meynert. Moreover, a significant increase in the number of small-sized neurons and a significant decrease in the number of large, putative cholinergic neurons could be detected, suggesting that apart from neuron loss neuron shrinkage appears to be another characteristic neuropathological feature of this degenerating cholinergic NBMC system. Preservation of these magnocellular cholinergic neurons in shrunken form renders it likely that cholinergic dysfunction, characteristic of Alzheimer's disease, may be responsive to neurotrophic influences.

Conjugate eye deviation: side, site, and size of the hemispheric lesion.

Conjugate eye deviation (CED) is a well-known sign that occurs rather frequently in stroke patients. To study the lateralizing and localizing value of this sign, we investigated prospectively 78 consecutive patients presenting with CED due to a hemispheric lesion. CED occurred more frequently after right-sided hemispheral damage (64%). The lesions in the right hemisphere were located predominantly in the subcortical (fronto-) parietal region and the internal capsule; the lesions in the left hemisphere were larger, covering the entire fronto-temporo-parietal area. In the majority of patients there was no direct involvement of the frontal eye fields on either side. The results indicate that a lesion at different sites within the circuit between the inferior parietal lobule and frontal eye fields, and their projections to the superior colliculus or paramedian pontine reticular formation, can be responsible for CED. The right-left asymmetry is probably related to cerebral asymmetry for directed spatial attention.

Cerebrospinal fluid rhinorrhea during treatment with bromocriptine for prolactinoma.

A 47-year-old man exhibited loss of libido and impotence in association with plasma hyperprolactinemia and a pituitary mass with downward extension of the tumor to the sphenoid sinus and to the suprasellar cisterns. Bromocriptine, 15 mg daily, reduced the hyperprolactinemia as well as tumor size. After 8 months on this therapy, the patient developed overt CSF liquorrhea. Five days after discontinuation of bromocriptine, the CSF rhinorrhea stopped, and when bromocriptine was given again 2 weeks later, CSF rhinorrhea returned within 3 days. We believe this phenomenon to be due to retraction of tumor by bromocriptine exposing a defect in the sella floor. Transient occurrence of CSF rhinorrhea can be considered as a consequence of tumor regression in patients on bromocriptine. The possibility of this complication, especially in patients with downward extension of tumor, should be noted.

Asymptomatic carotid bruit in patients who undergo coronary artery surgery.

The clinical significance of the presence of carotid bruit was evaluated in 643 patients who underwent coronary artery surgery alone or in combination with other cardiac procedures. Carotid bruit was heard in 31 patients (5%) who were neurologically asymptomatic. All of them underwent coronary artery surgery without additional carotid procedures, and none of them developed neurological deficits during the postoperative period. Of the remaining 612 patients, 18 were identified as having a history of focal neurological disorders, and 9 of them had carotid bruit. All were analyzed by means of noninvasive tests and angiography. Five underwent carotid endarterectomy prior to (2 patients) and simultaneously with (3 patients) a coronary bypass procedure. Seven patients developed neurological deficits postoperatively. Most of the deficits were not lateralized or focal but diffuse, which suggests global cerebral ischemia not related to carotid disease. Only 1 patient had proven carotid obstructive disease and underwent successful carotid thrombendarterectomy 10 days postoperatively. This study, although based on limited material, supports the hypothesis that patients with asymptomatic carotid bruit can safely undergo coronary artery surgery. In the group of patients without neurological symptomatology, postoperative neurological deficits were rarely caused by occlusive carotid disease. However, patients with asymptomatic carotid bruit should be closely followed with the goal of identifying those who are at risk of developing neurological deficits.

Clinical and electrophysiological study in a patient surviving from locked-in syndrome.

The results of clinical and electrophysiological investigations in a patient with a locked-in syndrome due to a pontine infarction, mainly on the right side, are presented. EEG showed only slight disturbances, while BAER and SSER revealed response alterations as could be expected from physical examination. BAER revealed altered central conduction after stimulation of either side. After median nerve stimulation on the right side SSER was slightly delayed, while no reproducible cortical response was seen after stimulation on the left side. Our patient survived and showed partial recovery.

Facial thermography in the diagnosis of cerebrovascular disease and in evaluation of carotid endarterectomy.

Some 60% of strokes are due to extracranial occlusive arterial lesions, most frequently at the bifurcation of the common carotid artery. Since these lesions are accessible to endarterectomy, their prestroke diagnosis is very important. Facial thermography quickly supplies reliqble information on the circulatory area in which these lesions occur, and this information can be atraumatically obtained in an out-patient setting. The success rate of facial thermography versus aortic arch angiography was 83% and 80%, respectively, in our case material, and this rate corresponds with data in the literature. In a series of 23 patients with facial thermograms and angiograms obtained before and after endarterectomy, facial thermography proved to be a useful diagnostic and prognostic aid in neurological out-patient guidance after carotid endarterectomy. By virtue of its rapidity and atraumatic character, because it can be carried out by technicians and because the findings are suitable for computer data processing, facial thermography would seem to be suitable for potential stroke screening of a high-risk asymptomatic population.

Course of blood pressure after cerebral infarction and transient ischemic attack.

In 63 patients, admitted for cerebral infarction or transient ischemic attack (TIA), the blood pressure course was studied. The blood pressure before the event was studied retrospectively; 32 patients were normotensive, in 31 patients existed hypertension, with antihypertensive treatment in 15 of these cases. The blood pressure after the event was studied prospectively, and turned out to be risen in 67% of the patients on the day of admission. It fell in the first day after infarction or TIA, mainly on the second day, to a plateau level reached on the fifth day. Only 3 patients (5%) remained hypertensive until discharge from the hospital. In 48 patients blood pressure values were available as measured two to six months after discharge, without a change in antihypertensive medication. Blood pressure was increased compared to the value measured before discharge. In 14 patients (29%) hypertensive blood pressure figures were measured at that time. It is concluded that blood pressure is elevated in the acute phase of cerebral infarction and TIA, but falls spontaneously in the first days to normotensive levels in most patients; because blood pressure may increase again, measurements of blood pressure within the first months after discharge are needed.

Blood pressure and both venous and urinary catecholamines after cerebral infarction.

Blood pressure, both venous and urinary catecholamines and plasma renin activity (PRA) were studied in 10 patients (6 men and 4 women, mean age 70 +/- 10 years) on the first three days after cerebral infarction. Blood pressure fell significantly (p less than 0.02) on the second and third day after stroke. There was a small but significant (p less than 0.01) decrease in plasma epinephrine concentration on the third day. The norepinephrine values remained constant on the three days. The PRA showed a significant (p less than 0.01) rise on the third day. No significant correlation was detected between the course of the blood pressure and the plasma catecholamines or PRA. When blood pressure was correlated with the urinary catecholamines, however, a significant correlation with epinephrine (r = 0.45; p less than 0.05) and with norepinephrine (r = 0.44; p less than 0.05) was found. We conclude that the changes in blood pressure after stroke are at least partly mediated by the changes in catecholamine production.

Neurologic manifestations of homocystinuria.

Recognition of the disease homocystinuria by the neurologist may be of importance as is illustrated in the dramatic case history of a 20 year old woman. Confusion with Marfan's syndrome frequently occurs. The clinical and pathologic anatomical features are described. A review of the literature is given and the use of contraceptives is discussed.

[Epidemiological aspects of stroke]. / Epidemiologische aspecten van de beroerte.

This article reviews some aspects of the descriptive neuro-epidemiology of stroke, paying special attention to the Netherlands. The steady decline of mortality and incidence of stroke is discussed. This temporal trend may be more influenced by changes in life style than by medical treatment.

[Consensus diagnosis in dementia syndrome]. / Consensus Diagnostiek bij het dementiesyndroom.

A consensus development conference held to reach agreement on definition, diagnostic criteria and clinical and ancillary investigations concerning the diagnosis of the dementia syndrome was convened in Utrecht by the National Organization for Quality Assurance in Hospitals in the Netherlands on November 4, 1988. Dementia was defined as a clinical syndrome diagnosable by clinical methods only. Its manifestation is primarily behavioural. It is characterized by a decline of two or more cognitive capacities, including memory, without alteration of consciousness, and by a significant disturbance of the usual daily activities of the patient. It was agreed that at present the DSM-III-R diagnostic criteria for dementia are the most acceptable, with the exception of one viz. evidence or presumption of an etiologic organic factor, because this criterion is not compatible with the syndromal character of the dementia syndrome. Consensus was also reached about the following statements. The diagnosis of dementia syndrome is not valid in the presence of delirium. For clinical reasons it is considered important to distinguish between the conditions of cortical and subcortical dementia. Pseudodementia is an out-of-date concept. Epidemiological data on dementia are important for the diagnosis and prognosis in individual cases. In all patients with signs of the dementia syndrome, physical, neurological, psychiatric, and neuropsychological examinations should be performed, preferably according to a standardized protocol. The etiologic role of drugs in the dementia syndrome and delirium in the aged cannot be overemphasized. For the differential diagnosis of the disease states that produce the dementia syndrome, standardized laboratory tests should always be performed, but with individual modifications. EEG and CT (or NMR) are appropriate in certain cases.

Prognostic significance of conjugate eye deviation in stroke patients.

We prospectively studied the prognostic significance of conjugate eye deviation in 80 patients with acute stroke and compared the 3-month mortality and disability of these patients to those of the Tilburg epidemiological study of stroke. Mortality of patients with conjugate eye deviation was higher (41%) than for the general stroke population (34%), but this difference was not statistically significant (p less than 0.179). Looking at mortality and disability together, we found the outcome of patients with conjugate eye deviation to be significantly worse (p less than 0.001). Deviation of the eyes occurred more frequently to the right (65%) than to the left (35%). In the patient group with eye deviation to the left, mortality was significantly higher (64%, p less than 0.001) than in the group with eye deviation to the right (25%); only two patients of the former group (n = 28) could return home. Compared to the Tilburg epidemiological study of stroke, the group with eye deviation to the left did significantly worse, both for mortality alone (p less than 0.001) and for mortality and disability together (p less than 0.001). The group with eye deviation to the right did significantly worse only for mortality and disability together (p less than 0.01). Our results indicate that conjugate eye deviation is a prognostic factor for poor short-term mortality and disability in stroke patients, especially when the eyes are deviated to the left.

Contribution of inappropriate treatment for hypertension to pathogenesis of stroke in the elderly.

One hundred and seventy eight patients admitted to hospital with acute cerebral infarction or transient ischaemic attack were studied to determine if their treatment had been changed during the previous three weeks and to compare their blood pressure after the stroke with premorbid values. Blood pressure measurements taken within one year before the stroke were available for 100 patients; seven of these had had a recent change in antihypertensive or diuretic treatment. Of these, three patients who had started taking frusemide because of hypertension and one whose dosage of a reserpine combination drug had been increased experienced an appreciable decrease in blood pressure immediately after the stroke; they also showed signs of haemoconcentration. The change in treatment probably contributed to the stroke in these four patients. The other three showed a smaller decrease or even an increase in blood pressure and no signs of haemoconcentration; the relation between the change in treatment and stroke is less likely in these patients. The use of high ceiling diuretics such as frusemide in the treatment of hypertension may induce hypovolaemia and hypotension, resulting in cerebral ischaemia, and are therefore best avoided in such treatment.