Rapidly progressive hippocampal atrophy: evidence for a seizure-induced mechanism.

Hippocampal formation atrophy (HFA) developed in an adult, who did not have epilepsy previously, after the occurrence of new-onset partial seizures from acute thrombosis of an ipsilateral parietal venous angioma. There was no evidence of hippocampal injury, and the patient had only one brief, generalized tonic-clonic seizure. Although HFA progressed rapidly over 5.5 months, the partial seizures did not become prolonged or secondarily generalized. Evidence from the patient indicates that partial seizure activity can cause rapid and progressive hippocampal atrophy.

Meningoencephalitis due to Blastomyces dermatitidis: case report and literature review.

Infection of the central nervous system by Blastomyces dermatitidis is a rare cause of meningoencephalitis. The existence of exclusive clinical infection of the meninges in the absence of pulmonary or other foci of infection has been debated. We describe a 20-year-old man presenting with meningoencephalitis caused by B dermatitidis. Blastomycotic infection was confirmed by isolation of the organism from brain tissue obtained at biopsy. Magnetic resonance imaging demonstrated progressive enhancement of basal meninges with involvement of bilateral basal ganglia and thalami. Treatment with amphotericin B arrested further neurologic decline. However, clinical and radiographic follow-up suggested damage to diencephalic structures. The diagnosis of blastomycotic meningoencephalitis is difficult to establish because no sensitive serologic test exists, and attempts to isolate the organism in cerebrospinal fluid obtained by lumbar puncture generally fail. A biopsy specimen of brain tissue is frequently necessary for the diagnosis. Survival is possible with timely initiation of therapy.

False subarachnoid hemorrhage in anoxic encephalopathy with brain swelling.

The authors present two comatose patients with brain swelling from anoxic encephalopathy. Nonenhanced computed tomography (CT) images showed increased density on the falx, on the tentorium, and in the basal cisterns, all of which falsely suggested subarachnoid hemorrhage. Autopsy in both patients failed to show subarachnoid hemorrhage. In rare circumstances, anoxic encephalopathy can mimic subarachnoid hemorrhage on nonenhanced CT.

Cerebral venous thrombosis complicated by hemorrhagic infarction: factors affecting the initiation and safety of anticoagulation.

BACKGROUND AND PURPOSE: Anticoagulation (AC) may improve outcome in cerebral venous thrombosis (CVT), even when complicated by pretreatment hemorrhagic infarction (HI). The HI characteristics which affect the decision to initiate AC therapy and its outcome are unknown. We reviewed our experience with AC treatment for patients with CVT and HI. METHODS: Retrospective study. RESULTS: Two groups of patients were compared: those who received AC (n = 6) and those who did not (n = 6). Hemorrhage volumes ranged from petechial to large (93 cm3) hematoma with mass effect. Anticoagulated patients received treatment a mean of 11.3 days after symptom onset. Each had exclusively extratemporal HI without midline shift and had stable hemorrhage volumes and clinical status for at least 24 h prior to AC. AC did not increase HI volume or worsen clinical outcome. All 6 non-AC patients had enlarging hematomas. Four of these 6 patients had temporal HI; and two required hematoma resection. CONCLUSIONS: AC therapy was avoided in CVT patients with HI that were located in the temporal lobe, caused midline shift or were enlarging. AC was safely initiated within several days in clinically stable patients with non-temporal-lobe HI of unchanging volume. We suggest that the location and unchanged volume on serial CT may be important factors influencing the safety of AC therapy in patients with CVT and HI.

Crossed cerebro-cellular diaschisis in a patients with melas with aphasia but without hemiparesis.

We describe a 25 year old woman diagnosed with MELAS during an acute stroke-like episode. Global aphasia, migraine-like headaches and hemi-anopsia were her main clinical features. MR imaging revealed extensive cortical and subcortical left hemispheric signal abnormalities. [Tc-99m]ECD SPECT scanning revealed crossed cerebrocerebellar diaschisis. Aphasia in the absence of gross hemiparesis can be related to cross-cerebellar diaschisis in MELAS.

Intra-arterial thrombolysis in acute basilar artery thromboembolism: the initial Mayo Clinic experience.

OBJECTIVE: To investigate the feasibility of intra-arterial thrombolysis in acute basilar artery thrombosis. DESIGN: We reviewed a consecutive series of patients in whom intra-arterial thrombolysis was performed during the period from 1994 to 1996. MATERIAL AND METHODS: Intra-arterial thrombolysis with urokinase was done in an attempt to recanalize the basilar artery in a series of nine patients with basilar artery thrombosis admitted to the neurologic intensive care unit. At the time of initial assessment, all nine patients had major neurologic deficits attributable to brain-stem ischemia, including two patients with locked-in syndrome. RESULTS: Recanalization of the basilar artery system was successful in seven of the nine patients (a range of 2 to 13 hours after the ictus). Failure to recanalize the basilar artery occurred in two patients, who died after progressing to coma. Complete recovery or only minimal neurologic deficits were demonstrated in five of the nine patients. Despite recanalization of the basilar artery, two patients had no major change in their neurologic function, and both ultimately had severe ataxia and were fully dependent on others. A cerebellar hemorrhage occurred in one patient but without clinical worsening. Two patients had a retroperitoneal hematoma. CONCLUSION: Intra-arterial thrombolysis with urokinase in acute basilar artery occlusion resulted in recanalization in seven of the nine patients (78%). Five of the nine patients recovered fully, including two patients who had had locked-in syndrome. In light of the devastating natural course of acute basilar artery occlusion, these initial results are encouraging and indicate that intra-arterial thrombolysis may be a useful emergency treatment, even in patients with prolonged symptoms of ischemia (up to 12 hours).

Multifocal brain MRI artifacts secondary to embolic metal fragments.

We report a patient with unusual MRI abnormalities that had the physical characteristics of ferromagnetic artifact. We believe that the MRI artifacts were due to microscopic embolic metal fragments, most likely from a mechanical heart valve prosthesis. Potential sources of metal emboli should be considered in patients with MRI abnormalities compatible with ferromagnetic artifact.

Endovascular treatment of cerebral aneurysms following incomplete clipping.

The authors report their experience using electrolytically detachable coils for the treatment of residual cerebral aneurysms following incomplete surgical clipping. Eight patients were treated for six anterior and two posterior circulation aneurysm remnants. All patients were referred for endovascular treatment by experienced cerebrovascular neurosurgeons at the authors' institution. Patients underwent follow-up angiography immediately after endovascular treatment. In seven of the eight patients, additional follow-up angiographic studies were obtained at periods ranging from 7 weeks to 2 years posttreatment. The latest follow-up angiograms demonstrated that six of the eight aneurysm remnants were 100% occluded, with near-complete occlusion of the other two aneurysm remnants. There was no permanent neurological or non-neurological morbidity or mortality associated with the treatment. There was no incidence of aneurysm hemorrhage during or after treatment. Endovascular treatment of cerebral aneurysm remnants following prior surgical clipping can be accomplished with acceptable morbidity and mortality rates. Endovascular coil occlusion can play an important adjunctive role in the treatment of those aneurysms that have been incompletely obliterated by surgical clipping.

Persistent cauda equina syndrome following bilateral aortoiliac dissection as a complication of cardiac angiography.

Cardiac angiography is accepted as an invasive yet safe procedure with well-characterized complications. We present a complication heretofore not described to our knowledge, in which a patient experienced the cauda equina syndrome following bilateral aortoiliac dissection during cardiac angiography. Similarities are noted between this complication and those documented in abdominal aortic aneurysm repair surgery.

Guillain-Barré syndrome.

The leading cause of acute neuromuscular weakness in the developed world is Guillain-Barré syndrome (GBS). Mortality rates vary widely. This article discusses the care and management of patients with GBS, with an emphasis on those patients who require admission to an intensive care unit.

The relationship between cerebral blood flow and transcranial Doppler blood flow velocity during hypothermic cardiopulmonary bypass in adults.

A noninvasive, simple, and continuous method to assess cerebral perfusion during cardiopulmonary bypass (CPB) could help prevent cerebral ischemia. Transcranial Doppler sonography (TCD) allows a noninvasive, on-line measurement of blood flow velocity in cerebral arteries. The correlation of TCD-estimated and actual cerebral blood flow (CBF) has not been well studied during CPB. We determined the correlation of middle cerebral artery (MCA) mean velocity and CBF determined by the Kety-Schmidt method during nonbypass and two hypothermic bypass flow conditions. Sixteen patients undergoing hypothermic (27 degrees C) CPB for coronary artery bypass grafting and/or valve replacement surgery were enrolled in the study. We were able to determine MCA velocity in only 12 patients. We determined CBF and MCA velocity in each patient during four 15-min study periods: 1) prebypass after sternotomy before aortic cannulation; 2) hypothermic (27 degrees C) CPB with 1.2 L.min-1.m-2 pump flow; 3) hypothermic CPB with 2.4 L.min-1.m-2 pump flow, and 4) 30 min after weaning from CPB. There was no difference in the mean arterial pressure between the two CPB pump blood flows. The pooled change in MCA velocity and CBF as percentage of baseline (prebypass) for all patients and at all time points had a correlation of 0.33 (r). A decrease or increase in MCA velocity did not necessarily indicate a corresponding decrease or increase in CBF. This technology may be of limited usefulness during the circulatory condition of hypothermic, nonpulsatile CPB.

Cure of a solitary brainstem abscess with antibiotic therapy: case report.

A solitary brainstem abscess is uncommon. The use of antibiotics and surgical aspiration or excision of a brainstem abscess has resulted in survivors. Survival after treatment of a brainstem abscess with antibiotics alone has been reported rarely, and we present the eighth study case. The patient made an excellent recovery after 12 weeks of antibiotics, with 8 weeks completed as an outpatient. Medical management of a solitary brainstem abscess in an immunocompetent patient is feasible and may result in a complete cure with antibiotics only. Completion of IV antibiotics as an outpatient is viable and cost-effective in selected patients.

Acute fatal deterioration in putaminal hemorrhage.

BACKGROUND: Clinical deterioration in patients with spontaneous intracerebral hemorrhage has rarely been studied. It has been previously thought that intracranial hematomas bleed in a monophasic fashion. Recent studies have demonstrated continuous active bleeding within hours after the event, resulting in enlargement of the hematoma. However, acute sudden and fatal deterioration suggesting a rebleed is rarely reported. SUMMARY OF REPORTS: An 84-year-old man was admitted with a moderate-size hemorrhage in the putamen and was treated for hypertension during the first day of admission. He acutely demonstrated extensor posturing and light-fixed pupils. Repeat CT scan showed massive enlargement of the intracranial hematoma and extension into the ventricles causing acute hydrocephalus. A 72-year-old man was admitted with a mid-size hemorrhage in the putamen. Acute deterioration with loss of all brain stem reflexes except for cornea reflexes was associated with a large increase in volume of the hematoma, 7 hours after the initial hemorrhage. An 85-year-old woman was admitted with a small hemorrhage in the putamen and recovered to be able to walk unassisted. She suddenly died from a recurrent massive putaminal hemorrhage 2 weeks after the ictus. CONCLUSIONS: Patients with spontaneous intracerebral hemorrhage in the putamen may die acutely from fatal catastrophic enlargement of the initial hematoma hours to days after the ictus. In some patients with spontaneous intracerebral hemorrhage and clinical deterioration, rebleeding may be a possible mechanism.

Western Nebraska family (family D) with autosomal dominant parkinsonism.

The etiology of Parkinson's disease (PD) remains uncertain. Environmental influences may have an important role, but genetic factors have been firmly implicated in several recently reported kindreds. We studied a family (family D) whose ancestors probably immigrated to the United States from England. The pedigree contains 188 individuals spanning six generations with 18 affected members. Autosomal dominant inheritance is present. Typical levodopa-responsive PD with bradykinesia, rigidity, resting tremor, and impaired postural reflexes develops. Eye movement abnormalities, pyramidal and cerebellar signs, sensory disturbances, and orthostatic blood pressure changes do not occur. Disease progression is slow. PET with [18F]-6-fluoro-L-dopa (FD) performed on an affected individual revealed decreased uptake of FD in a pattern consistent with PD. Autopsy performed on another affected individual demonstrated neuronal and pigmentary loss, gliosis, and Lewy bodies in the substantia nigra pars compacta. This large kindred appears to represent a neurodegenerative disorder closely resembling, if not identical to, idiopathic PD.

Gastrointestinal bleeding in stroke.

BACKGROUND AND PURPOSE: Patients with ischemic or hemorrhagic stroke are at risk for systemic complications. The reasons why gastrointestinal bleeding occurs after stroke are unknown and have intuitively been attributed to stress ulcers. No study to date has addressed causes of gastrointestinal hemorrhage in stroke. METHODS: Between 1976 and 1994, 17 patients identified from the Mayo Clinic medical record system as having gastrointestinal hemorrhage and ischemic stroke (n = 14) or intracerebral hemorrhage (n = 3) were reviewed for presentation, associated causes, and outcome. Results of the endoscopic procedures were compiled, and available gastric biopsies were reviewed. RESULTS: In 17 patients with gastrointestinal bleeding after stroke, sudden hematemesis, a decrease in hemoglobin level, or orthostatic hypotension was found as a presenting feature. One patient presented with massive hematemesis, exsanguination, and cardiac arrest. Endoscopic findings were available in 14 patients and included gastroesophageal erosions, hemorrhagic gastritis, and gastric ulcer. In one patient, an adenocarcinoma of the gastric cardia was found. Putative pathogenetic agents were found in 16 of 17 patients and included a long history of nonsteroidal anti-inflammatory drugs (n = 6), acetylsalicylic acid (n = 3), grossly prolonged anticoagulation (n = 4), Helicobacter pylori (n = 2), and corticosteroids (n = 1). CONCLUSIONS: Gastrointestinal bleeding after stroke is rarely severe and may not contribute significantly to mortality. Medication-induced gastrointestinal hemorrhage may be underappreciated in this setting.