Bilateral paramedian thalamic infarct in the presence of an unpaired thalamic perforating artery.

Bilateral paramedian thalamic infarction is rare. The suggested mechanism is occlusion of a central unpaired thalamic perforating artery--an anatomic variant. In the few existing reports of this condition, the diagnosis was based on computed tomography (CT) or magnetic resonance imaging (MRI) findings alone. Other causes of thalamic lesions were not ruled out, and there was no angiographic demonstration of the presumed variant artery. We present a case of a 48-year-old man with a bilateral thalamic infarction seen on CT and MRI. Initial neurological examination revealed lethargy, severe combined motor and sensory aphasia, and a mild upward gaze limitation. The patient had no focal motor deficits. After 24 hours, the patient was more alert and his speech became more fluent, but Korsakoff-type amnesia with poor attention span became apparent. The patient improved slowly over 6 months of rehabilitation. Bilateral thalamic lesions can be caused by several conditions. Among those are thiamine deficiency, cerebral lupus, toxoplasmosis, cysticercosis, cerebral syphilitic gumma, and even tumors and fungal infections. All these were ruled out in our case. Superselective digital subtraction angiography (DSA) demonstrated a single unpaired thalamic perforator. To our knowledge, this is the first time this anatomical variant has been demonstrated in vivo in association with bilateral thalamic infarction.

Bedside external ventricular drain placement for the treatment of acute hydrocephalus.

The purpose of this retrospective study was to evaluate the results of external ventricular drain (EVD) placement for the management of hydrocephalus. We present our experience with 103 consecutive cases over one year, 56 of which had subarachnoid hemorrhage (SAH). Short tunnel ventriculostomy was performed at the bedside in the neurosurgical intensive care unit (NSICU), using sterile technique. Long-term care included meticulous site care by a dedicated NSICU nurse, daily cultures and prophylactic antibiotics. The average duration of EVD was 10.7 days (range 1-28 days). There was one case of positive cerebrospinal fluid (CSF) culture. Additional complications included one small intraparenchymal hematoma and two cases of EVD disconnection. No patient died form EVD-associated complications. No rebleed from aneurysmal SAH was seen. There was no correlation between the duration of EVD and infection. We conclude that placement of short EVD in the NSICU is safe and can be maintained for the required duration of treatment with minimum infection rate.

Neurodegeneration prevented by lentiviral vector delivery of GDNF in primate models of Parkinson's disease.

Lentiviral delivery of glial cell line-derived neurotrophic factor (lenti-GDNF) was tested for its trophic effects upon degenerating nigrostriatal neurons in nonhuman primate models of Parkinson's disease (PD). We injected lenti-GDNF into the striatum and substantia nigra of nonlesioned aged rhesus monkeys or young adult rhesus monkeys treated 1 week prior with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Extensive GDNF expression with anterograde and retrograde transport was seen in all animals. In aged monkeys, lenti-GDNF augmented dopaminergic function. In MPTP-treated monkeys, lenti-GDNF reversed functional deficits and completely prevented nigrostriatal degeneration. Additionally, lenti-GDNF injections to intact rhesus monkeys revealed long-term gene expression (8 months). In MPTP-treated monkeys, lenti-GDNF treatment reversed motor deficits in a hand-reach task. These data indicate that GDNF delivery using a lentiviral vector system can prevent nigrostriatal degeneration and induce regeneration in primate models of PD and might be a viable therapeutic strategy for PD patients.

Giant anterior communicating artery aneurysm infiltrated with a primary cerebral lymphoma: case report.

OBJECTIVE AND IMPORTANCE: Central nervous system lymphomas exhibit angiotropic characteristics. Nevertheless, direct association with an intracranial aneurysm is very rarely reported. We present a case of a giant aneurysm infiltrated with a large cell non-Hodgkin's lymphoma. The incidence of primary central nervous system lymphoma is increasing, and similar cases may become more frequent in the future. CLINICAL PRESENTATION: A 65-year-old man had presented with a giant anterior cerebral artery aneurysm, new onset of seizures, aphasia, and hemiparesis. The aneurysm was treated with Guglielmi detachable coils. Six months later, the patient exhibited fever and neurological deterioration. Magnetic resonance images suggested an enhancing lesion posterior to the neck of the aneurysm. Antibiotic treatment given elsewhere was unsuccessful. INTERVENTION: A craniotomy for a suspected abscess was performed, with removal of the aneurysm and clipping of the neck. The aneurysm sac appeared to be filled with thrombus and pus. The results of aerobic, anaerobic, and fungal cultures were negative. Postoperative magnetic resonance images demonstrated a residual mass, posterior to the aneurysm within the striatum and the internal capsule. Histological examination of the aneurysm wall revealed a large B-cell lymphoma. The diagnosis was confirmed by a stereotactic biopsy. Radiation therapy resulted in a transient decrease in the size of the lesion. CONCLUSION: Although the tumor was not apparent on the initial imaging studies, it may have been the cause of the patient's presenting symptoms. Infiltration of the aneurysm wall by the lymphoma also raises the possibility of a causal relationship. As the incidence of primary central nervous system lymphoma is reported to be on the increase, awareness this uncommon association of an aneurysm and malignant lymphoma is of value.

Delayed onset of progressive dystonia following subacute 3-nitropropionic acid treatment in Cebus apella monkeys.

Delayed abnormal movements can be observed in patients with acute neurologic insult after a prolonged period of apparent neurologic stability. To reproduce such a secondary neurologic manifestation in primates, the present experiment investigated whether systemic administration of subacute 3-nitropropionic acid (3NP), a mitochondrial toxin, could induce abnormal movements that were delayed and progressive over time. Four Cebus apella monkeys received systemic 3NP injections until acute neurologic signs manifested. The monkeys were regularly video-recorded and rated for abnormal movements for up to 15 weeks after the cessation of 3NP treatment. Five to 6 weeks after the 3NP treatment, monkeys displayed a significant increase in dyskinesias compared with pretreatment conditions. Over time the chorea attenuated, whereas the dystonic movements increased in intensity and severity which was characterized by a delayed decrease of peak tangential velocity. The intensity of abnormal movements and extent of affected body regions observed in each monkey were consistent with the size of basal ganglia hypersignal as documented by T2 sequence on magnetic resonance imaging. Thus, more severe motor impairments were associated with large magnetic resonance image abnormalities. This novel primate model may be particularly useful for studying the structural changes underlying delayed and progressive manifestations of abnormal movements with the ultimate goal of facilitating the evaluation of novel therapeutic strategies.

Lentiviral gene transfer to the nonhuman primate brain.

Lentiviral vectors infect quiescent cells and allow for the delivery of genes to discrete brain regions. The present study assessed whether stable lentiviral gene transduction can be achieved in the monkey nigrostriatal system. Three young adult Rhesus monkeys received injections of a lentiviral vector encoding for the marker gene beta galatosidase (beta Gal). On one side of the brain, each monkey received multiple lentivirus injections into the caudate and putamen. On the opposite side, each animal received a single injection aimed at the substantia nigra. The first two monkeys were sacrificed 1 month postinjection, while the third monkey was sacrificed 3 months postinjection. Robust incorporation of the beta Gal gene was seen in the striatum of all three monkeys. Stereological counts revealed that 930,218; 1,192,359; and 1,501,217 cells in the striatum were beta Gal positive in monkeys 1 (n = 2) and 3 (n = 1) months later, respectively. Only the third monkey had an injection placed directly into the substantia nigra and 187,308 beta Gal-positive cells were identified in this animal. The injections induced only minor perivascular cuffing and there was no apparent inflammatory response resulting from the lentivirus injections. Double label experiments revealed that between 80 and 87% of the beta Gal-positive cells were neurons. These data indicate that robust transduction of striatal and nigral cells can occur in the nonhuman primate brain for up to 3 months. Studies are now ongoing testing the ability of lentivirus encoding for dopaminergic trophic factors to augment the nigrostriatal system in nonhuman primate models of Parkinson's disease.

Abdominal cerebrospinal fluid pseudocyst: A complication of ventriculoperitoneal shunt in children.

The present paper is a retrospective analysis of 27 consecutive patients, treated for abdominal cerebrospinal fluid (CSF) pseudocyst at the Children's Memorial Hospital in the years 1991-1996. This series is compared to the previous experience from our institution. Treatment consisted of the removal of the ventriculoperitoneal (VP) shunt and placement of an external ventricular drain. Antibiotics were administered intravenously for 10 days. The cysts were aspirated intraoperatively in 9 patients and postoperatively with ultrasound guidance in 3 patients, while they resolved spontaneously in 15 others. In 21 of 27 cases (78%), the shunt could be reinserted into the abdomen in a new location. Four patients had a ventriculopleural shunt, and in 2 patients, a ventriculoatrial shunt was inserted. Forty-four percent of the patients had a positive culture on presentation. The positive culture rate was 77% for those 4 years old and younger and only 28% for those aged 5 and above (p = 0.03). We conclude that abdominal CSF pseudocysts are resolved by externalizing the shunt. A VP shunt can be safely reinserted in the majority of the patients. Infection, while an important factor, is not likely to account for all cases of pseudocyst.