Hypocretin-1 levels in the cerebrospinal fluid of patients with Percheron artery infarction with or without midbrain involvement: A case series.

BACKGROUND: Bilateral paramedian thalamic infarctions (BPTIs) due to artery of Percheron occlusion are known to cause hypersomnia. However, the role of hypocretin-1, a wake-promoting peptide that is located at the lateral hypothalamus, in hypersomnia in these patients remains unclear. METHODS: To clarify the role of hypocretin-1 in hypersomnia in patients with BPTIs, hypocretin-1 levels in the cerebrospinal fluid (CSF) were measured in 6 patients with BPTIs: 2 with rostral midbrain involvement (BPT+RMI) and 4 without midbrain involvement (BPT-MI). RESULTS: CSF hypocretin-1 levels were decreased in 2 patients with BPT+RMI and were within normal ranges in 4 patients with BPT-MI. Hypersomnia was noted in all the patients. In one BPT+RMI patient, hypersomnia was improved within 2 weeks and decreased CSF hypocretin-1 levels were reversed (acute phase (on day 9), 109.2 pg/mL; chronic phase (at 3 months), 323 pg/mL), whereas another BPT+RMI patient who displayed coma in the acute phase had decreased CSF orexin levels (107 pg/mL) at day 49 and exhibited severe disability. CONCLUSION: Hypocretin deficiency was not involved in hypersomnia observed in BPT-MI patients; however, CSF hypocretin-1 levels were reduced in BPT+RMI patients. Reduced CSF hypocretin-1 levels in the chronic phase may possibly predict a poor clinical outcome in patients with Percheron artery infarction.

Improved outcome of patients with severe thalamic hemorrhage treated with cerebrospinal fluid drainage and neurocritical care during 1990-1994 and 2005-2009.

INTRODUCTION: Patients with thalamic hemorrhage, depressed level of consciousness and/or signs of elevated intracranial pressure may be treated with neurocritical care (NCC) and external ventricular drainage (EVD) for release of cerebrospinal fluid. METHODS: Forty-three patients with thalamic hemorrhage treated with NCC from 1990 to 1994 (n = 21) and from 2005-2009 (n = 22) were evaluated. Outcome was assessed using the Glasgow Coma Scale (GCS) score at discharge from our unit and the modified Rankin Scale (mRS) for long-term outcome. RESULTS: Patients' age was 59.5 ± 7 years in 1990-1994, and 58.2 ± 9 years in 2005-2009. The median (25th and 75th percentile) GCS score on admission for the two time periods was 9 (6-12) and 9 (4-14), respectively. Long-term follow-up was assessed at a mean of 37.1 (range 19-65) months after disease onset for the 1990-1994 cohort and at 37.4 (range 14-58) months for the 2005-2009 cohort. Compared to patients from 1990 to 1994, patients from 2005 to 2009 had a significantly better outcome (median mRS [25th and 75th percentile]: 5 [4-6] vs. 4 [2-4.5]; p < 0.01). Most patients (13/21, 62 %) treated from 1990 to 1994 had unchanged or lower GCS scores during their NCC stay in contrast to 7/22 (32 %) from 2005 to 2009. At the last follow-up, 13/21 (62 %) patients from 1990 to 1994 were dead in comparison to 4/21 (19 %) from 2005 to 2009 (p < 0.05). Negative prognostic factors were the 120 h post-admission GCS score in the 1990-1994 patient cohort (p = 0.07) and high age in the recent cohort (p = 0.04). CONCLUSIONS: Patients with thalamic hemorrhage and depressed level of consciousness on admission had a worse outcome in the early 1990s compared with the late 2000s, which may at least be partially attributed to refined neurocritical care.

Bilateral thalamic lesions.

OBJECTIVE: Bilateral thalamic lesions are rare and relatively obscure neoplasms. We present our experience with nine cases of bilateral thalamic lesions and attempt to analyse them in the background of available literature. MATERIALS AND METHODS: Retrospective analyses of the case records of 9 cases of bilateral thalamic lesions treated in our department since January 2002, which have a minimum of 1 year follow-up. RESULTS: The study group included four males and five females with a mean age of 14.6 years (5 years to 29 years). Seven of these patients had radiological evidence of bilateral thalamic lesions at presentation and 2 patients had involvement of the opposite thalamus at a later stage of the disease. All patients except one presented with raised intracranial pressure symptoms. Focal motor deficits (4/9), behavioral and memory disturbances (3/9) were the other major presenting symptoms. Biopsy confirmation was possible in six patients and histopathology was suggestive of low grade fibrillary astrocytoma in all six patients. Seven patients required CSF diversion procedure for associated hydrocephalus. Eight of our nine patients underwent radiotherapy. On last follow-up, 3 patients were clinically stable with images suggestive of arrested disease, four patients had evidence of progressive disease both clinically and radiologically and there were two recorded cases of mortality. CONCLUSION: Primary bilateral thalamic lesions have characteristic neuroradiological properties and are distinct from unilateral thalamic tumours with bilateral progression. Almost all of these lesions on histology prove to be gliomas but decompressive surgery is seldom feasible. Surgical intervention is limited to biopsy and CSF diversion for hydrocephalus. Bilateral thalamic lesions remain unresponsive to adjuvant therapy and generally carry a poor prognosis.

Hemiballismus: changes in cerebrospinal fluid.

Concentrations of serotonin metabolite, 5-hydroxyindoleacetic acid (5-HIAA), and dopamine metabolites, homovanillic acid (HVA) and 3,4-dihydroxy-phenylacetic acid (DOPAC), were measured in the samples of cerebrospinal fluid of 5 patients with acute hemiballismus. The only significant change was the increased content of HVA compared to controls. This finding support the hypothesis on the increased dopamine turnover in hemiballismus and provide a rational basis for the present treatment with antidopaminergic agents.