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Both programs allowed statistical differentiation between Parkinson's syndrome and essential tremor. Strict operator protocols are needed with QuantiSPECT to reduce inter- and intra-operator variation. The three-dimensional method (BRASS) gave greater concordance than the two-dimensional method (QuantiSPECT) with the visual assessment, but at a cost of increased operator time.

Background: Zolpidem is an omega 1 specific indirect GABA agonist that is used for insomnia, but may have efficacy in brain damage. The long term efficacy of zolpidem in the permanent vegetative state is described in three patients. Method: Two motor vehicle accident patients and one near drowning patient, all of them in the permanent vegetative state for at least three years, were rated according to the Glasgow Coma and Rancho Los Amigos scale before and after zolpidem application. Long term response to daily application of this drug was monitored for 3-6 years. Results: All patients were aroused transiently every morning after zolpidem. Glasgow Coma Scale scores ranged from 6-9/15 before to 10-15/15 after zolpidem. Rancho Los Amigos Cognitive scores ranged from I-II before to V-VII afterward. Drug efficacy did not decrease and there were no long term side effects after 3-6 years daily use. Conclusion: Zolpidem appears an effective drug to restore brain function to some patients in the permanent vegetative state.

During 15 years, 23 clinical reports and 6 studies have demonstrated associations between sub-sedative doses of zolpidem and recoveries from brain damage due to strokes, trauma and hypoxia. Clinical findings include unexpected awakenings from vegetative states and regressions of stroke symptoms after dosing that disappear during elimination and reappear on repeat dosing. Initially single-photon emission computed tomography scans showed improved perfusion within, around and distant from infarctions. Then positron emission tomography scans and electroencephalography detected renewed metabolic and neuronal activity. Placebo or a similar, gamma-aminobutyric acid (GABA)-ergic, sedative zopiclone has no such effect. The effect appears only several months after the injury, reflecting recent evidence in mice of substantial differences between the states of GABA receptors in acute and chronic repair phases of recovery. Zolpidem's good safety record and rapid absorption further indicate a need for more clinical trials. List of acronyms: BOLD, Blood-Oxygen-Level Dependent contrast imaging in MRI; CRS, Coma Recovery Scale; CRS-R, Coma Recovery Scale Revised; CSI, Cerebral State Index; CSM, Cerebral State Monitor; DOC, Disorder of Consciousness; EEG, Electro Encephalography; FDG-PET, FluoroDeoxyGlucose-Positron Emission Tomography; FTD, Frontotemporal dementia; GABA, Gamma-Aminobutyric Acid; MCS, Minimally Conscious State; M-EEG, Magneto-Encephalography; MRI, Magnetic Resonance Image; MSN, Median Spiny Neurones; PET, Positron Emission Tomography; PVS, Persistent Vegetative Sate; RLAC, Rancho Los Amigos Cognitive scores; SPECT, Single-photon emission computed tomography; TFES, Tinetti Falls Efficacy Scale; 99mTc HMPAO, Technetium hexamethylpropyleneamine oxime.

to the editor: There is currently no effective pharmacologic treatment for spinocerebellar ataxia. We describe a family of five patients, four of whom had clinical improvement within one hour after the ingestion of zolpidem (10 mg). The diagnosis of spinocerebellar ataxia type 2 was confirmed by molecular analysis. Analysis of DNA for CAG repeat expansions in the SCA1 , 2 , 3 , 6 , and 7 genes revealed expansion of CAG repeats at the SCA2 locus.Patient 1, a 49-year-old man with titubation, dizziness, and loss of balance from the age of 34 years, had deteriorating speech and handwriting. Cerebellar signs included moderate gait ataxia, intention tremor, and dysdiadochokinesis, as well as titubation. Deep-tendon reflexes were all brisk. After treatment with zolpidem, ataxia, intention tremor, and titubation improved moderately. Pollock Park Family Practice Springs 0084, South Africa 1. Salva P, Costa J. Clinical pharmacokinetics and pharmacodynamics of zolpidem: therapeutic implications. Clin Pharmacokinet 1995;29:142-53. 2. Thomas P, Rascle C, Mastain B, Maron M, Vaiva G. Test for catatonia with zolpidem. Lancet 1997;349:702. 3. Clauss RP, Güldenpfennig WM, Nel HW, Sathekge MM, Venkannagari RR. Extraordinary arousal from the semi-comatose state on zolpidem: a case report. S Afr Med J 2000;90:68-72. 4. Cohen L, Chaaban B, Habert M-O. Transient improvement of aphasia with zolpidem. N Engl J Med 2004;350:949-50. 5.Clauss RP, Nel HW. The effect of zolpidem on brain injury and diaschisis as detected by 99mTc HMPAO brain SPECT in humans. Arzneimittelforschung (in press). Correspondence