Abdominal decompression illness following repetitive diving: a case report and review of the literature.

The complete pathophysiology of decompression illness is not yet fully understood. What is known is that the longer a diver breathes pressurized air at depth, the more likely nitrogen bubbles are to form once the diver returns to surface [1]. These bubbles have varying mechanical, embolic and biochemical effects on the body. The symptoms produced can be as mild as joint pain or as significant as severe neurologic dysfunction, cardiopulmonary collapse or death. Once clinically diagnosed, decompression illness must be treated rapidly with recompression therapy in a hyperbaric chamber. This case report involves a middle-aged male foreign national who completed three dives, all of which incurred significant bottom time (defined as: "the total elapsed time from the time the diver leaves the surface to the time he/she leaves the bottom)" [2]. The patient began to develop severe abdominal and back pain within 15 minutes of surfacing from his final dive. This case is unique, as his presentation was very concerning for other medical catastrophes that had to be quickly ruled out, prior to establishing the diagnosis of severe decompression illness. After emergency department resuscitation, labs and imaging were obtained; abdominal decompression illness was confirmed by CT, revealing a significant abdominal venous gas burden.

Intracerebral abscess: a complication of severe cystic fibrosis lung disease.

Intracerebral abscess is an uncommon complication of severe cystic fibrosis lung disease. The present report describes a case of fatal multiple intracerebral abscesses in a patient with a severely bronchiectatic, nonfunctioning right lung and chronic low-grade infection. The patient was previously turned down for pneumonectomy. Intracerebral abscess in cystic fibrosis and the potential role of pneumonectomy in the present patient are discussed.

Globus pallidus dopamine and Parkinson motor subtypes: clinical and brain biochemical correlation.

BACKGROUND: Patients with Parkinson disease (PD) may be akinetic/rigid, be tremor dominant, or have comparable severity of these motor symptoms (classic). The pathophysiologic basis of different PD phenotypes is unknown. This study assessed pallidal and striatal dopamine level patterns in different motor subgroups of PD and normal control brains. METHODS: Globus pallidus and striatum dopamine (DA) levels were measured with high performance liquid chromatography in eight autopsy confirmed PD and five control frozen brains. RESULTS: DA levels in the external globus pallidus (GPe) of normal brains were nearly six times greater than in the internal pallidum (GPi). In PD, the mean loss of DA was marked (-82%) in GPe and moderate (-51%) in GPi. DA loss of variable degree was seen in different subdivisions of GPe and GPi in PD; however, DA levels were near normal in the ventral (rostral and caudal) GPi of PD cases with prominent tremor. There was marked loss of DA (-89%) in the caudate and severe loss (-98.4%) in the putamen in PD. The pattern of pallidal DA loss did not match the putaminal DA loss. CONCLUSION: There is sufficient loss of dopamine (DA) in external globus pallidus and the internal globus pallidum (GPi) as may contribute to the motor manifestations of Parkinson disease (PD). The possible functional disequilibrium between GABAergic and DAergic influences in favor of DA in the caudoventral parts of the GPi may contribute to resting tremor in tremor dominant and classic PD cases.

Is levodopa toxic to human substantia nigra?

Levodopa (LD) is the most effective drug for symptomatic control of Parkinson's disease, but has been suspected to be toxic to substantia nigra (SN) dopaminergic neurons. Tissue culture and animal studies of LD toxicity have produced contradictory evidence, and one study reported that a human subject exposed to a large cumulative dose (cd) of LD over 4 years had no evidence of SN damage. We report the cases of five patients, each of whom received a large cd of LD over a long period. Fluorodopa positron-emission tomography performed in one case indicated parkinsonism. Autopsies in two cases indicated a normal SN in one and a hypopigmented SN with normal cell complement in the other. Three patients had essential tremor, one had nonprogressive parkinsonism, and one had dopa-responsive dystonia. LD (without decarboxylase inhibitor) was administered over 21 years (cd = 21.99 kg), 9 years (cd = 6.6 kg), 26 years (cd = 18.7 kg), 11 years (cd = 3 kg), and 26 years (cd = 23.93 kg), respectively. None of the patients with essential tremor developed clinical features of parkinsonism that indicated significant SN damage, and one had a normal SN at autopsy. The parkinsonian patient displayed no detectable acceleration of disease process, and the patient with dopa-responsive dystonia had a normal complement of SN neurons at autopsy. We conclude that LD, administered at a dose commonly used for treating Parkinson's disease, was not toxic to SN neurons in these cases.

Concordance of common movement disorders among familial cases.

Multicase families are frequently utilized in studies of movement disorders (MDs). We report families with two or more MD cases seen at the Movement Disorder Clinic, Saskatoon (MDCS). In 30% of the MD probands, there was either a history or documentation of at least one secondary MD case in the family. Only those MD cases that were seen at the MDCS were considered in this study. A total of 56 probands and 77 secondary MD cases were seen at the MDCS between 1968 and 1996. In 24 (31.2%) of the secondary cases, the diagnosis was different from that in the proband. In 46 families (82%), only one secondary case was seen, and the diagnosis was concordant with the proband in 71.7%. In the remaining 10 families with two or more secondary cases, the diagnosis was concordant in 64.5% of cases. The largest subgroup was Parkinson's disease (PD)--40 probands and 53 secondary cases. of these secondary cases, 73.6% had PD. The concordance rate was 91% in essential tremor, but only 12.5% if the proband had essential tremor + parkinsonism. Considering that a large proportion of secondary cases have a diagnosis discordant with the proband, we recommend that, whenever possible, MD diagnosis in secondary cases be based on clinical assessment.

Amantadine effectiveness in multiple system atrophy and progressive supranuclear palsy.

Progressive Supranuclear palsy (PSP) and multiple system atrophy (MSA) each respond poorly to most anti-parkinsonian drugs. We assessed PSP and MSA cases seen between 1970 and 1996 for response to amantadine (Amd) 100 mg twice daily. Of 13 MSA cases (six females, seven males), eight (61.5%) improved, four (30.8%) did not benefit and one had insufficient documentation. Adverse effects were observed in three (23.1%) cases. Of 14 PSP (three females, 11 males), six (42.9%) had some improvement, five (35.7%) had no benefit, and three (21.4%) had inadequate documentation. Adverse effects were noted in three (28.6%) cases. Improvement is likely related to NMDA antagonist properties of Amd. We recommend consideration of Amd in the management of both PSP and MSA.