Acute spinal cord compression caused by disseminated Nocardia infection involving the conus medullaris.

Distinguishing between an infective and malignant process provides a diagnostic challenge for clinicians. This case highlights an example of an acute spinal cord compression that could fall into either of these two categories. The diagnosis in this case of disseminated Nocardiosis is an extremely rare cause of acute spinal cord compression and to our knowledge intrinsic conus medullaris infection from Nocardia has not previously been reported in the literature. Nocardia cyriacigeorgica is an emerging strain of Nocardia species recently identified which was previously categorised as Nocardia asteroides type VI infection. The challenge of eliciting the diagnosis and the need to have an index of suspicion of Nocardia as a possible aetiology agent is shown in the report. The case shows this is especially important in evaluation of a multi-system infection in an immunosuppressed individual. The case described highlights an interesting diagnostic case with the resultant causative organism an emerging strain of Nocardia species with no previous reported cases of conus medullaris involvement.

Effects of short-chain fatty acid-supplemented total parenteral nutrition on intestinal pro-inflammatory cytokine abundance.

We examined the effect of short-chain fatty acid-supplemented total parenteral nutrition on proinflammatory cytokine levels in piglets. Piglets (N = 22) received either standard total parenteral nutrition or total parenteral nutrition supplemented with short-chain fatty acids. After seven days of continuous nutrient infusion, proinflammatory cytokine (TNF-alpha, IL-1beta, IL-6) abundance in plasma, jejunal, and ileal samples and small intestinal myeloperoxidase was determined using western blotting. No differences were seen in TNF-alpha small intestinal abundance. IL-1beta was higher in the small intestine of the short-chain fatty acid group (P < 0.05). IL-6 was higher in intestinal samples of the short-chain fatty acid group (P = 0.05), with the ileum having a greater abundance of IL-6 than the jejunum (P < 0.005). No differences in proinflammatory cytokine abundance in the plasma or tissue myeloperoxidase were seen. These results indicate short-chain fatty acids beneficially increase small intestinal abundance of IL-1beta and IL-6 during total parenteral nutrition administration, while not affecting systemic production of these cytokines or intestinal inflammation.

Myostatin, insulin-like growth factor-1, and leukemia inhibitory factor mRNAs are upregulated in chronic human disuse muscle atrophy.

Human disuse muscle atrophy frequently accompanies orthopedic injury, arthritis, or bed rest, and recovery is often incomplete despite current rehabilitation programs. We have studied the vastus lateralis muscle in 12 patients with chronic disuse atrophy associated with chronic osteoarthritis of the hip both preoperatively and after total hip arthroplasty. Semiquantitative reverse transcriptase-polymerase chain reaction (RT-PCR) demonstrated an increase in the level of expression of myostatin, insulin-like growth factor-1 (IGF-1) and leukemia inhibitory factor (LIF) mRNAs compared to healthy control muscle. In all patients there was a significant correlation preoperatively between increasing myostatin mRNA expression and reduction in type 2A and 2B fiber area. In the 8 female patients there was a significant correlation between increased myostatin mRNA expression and the atrophy factor calculated for 2A and 2B fiber types preoperatively. We hypothesize that a complex interaction occurs between muscle growth regulating factors in the genesis of muscle wasting. Our results indicate that myostatin is a muscle-wasting factor contributing to type 2B and 2A atrophy. Other muscle growth factors, such as IGF-1 and LIF, may be upregulated in a counterregulatory fashion or may be involved in the fiber type switching seen in disuse muscle wasting.

Increased levels of leukemia inhibitory factor mRNA in muscular dystrophy and human muscle trauma.

Leukemia inhibitory factor (LIF) is an important muscle trauma factor both after crush injury and in the mdx mouse dystrophy model. It is important to establish which growth factors have a role in human muscle regeneration due to potential clinical therapeutic applications. As there is limited information concerning LIF expression in human muscle, we investigated the relative levels of LIF messenger ribonucleic acid (mRNA) in human muscle injury. Semiquantitative reverse transcriptase followed by polymerase chain reaction was used to amplify LIF message. We found that although LIF mRNA is expressed in low levels in control muscle, a sevenfold increase occurred after orthopedic muscle trauma and a marked 19-fold increase in dystrophic muscle (P < 0.002). These results indicate that LIF mRNA is upregulated in surgical and especially medical muscle injury with repeated myonecrosis. Muscle growth factors such as LIF may assist in future muscle rehabilitation after injury.

The angiotensin converting enzyme (ACE) inhibitor, perindopril, modifies the clinical features of Parkinson's disease.

BACKGROUND: Animal studies have demonstrated an interaction within the striatum between the angiotensin and dopaminergic systems. In rats, the angiotensin converting enzyme (ACE) inhibitor, perindopril, crosses the blood brain barrier and increases striatal dopamine synthesis and release. In humans, angiotensin type 1 receptors have been found on dopaminergic neurons in the substantia nigra and striatum. In Parkinson's disease, there is a marked reduction of these receptors associated with the nigrostriatal dopaminergic neuron loss. AIMS: We performed a double blind placebo controlled crossover pilot study in seven patients to investigate the effect of the ACE inhibitor, perindopril on the clinical features of moderately severe Parkinson's disease. RESULTS: After a four week treatment period with perindopril, patients had a faster onset in their motor response to L-dopa and a reduction in 'on phase' peak dyskinesia, p=0.021 and p=0.014 respectively. Patients also reported more 'on' periods during their waking day in their movement diary, p=0.007. Perindopril was well tolerated without any significant postural hypotension or renal dysfunction. CONCLUSIONS: These results suggest that ACE inhibitors such as perindopril may have a place in the management of motor fluctuations and dyskinesia in Parkinson's disease and justify further study.

Evolution of motor fluctuations in Parkinson's disease: a longitudinal study over 6 years.

A prospective longitudinal 6-year study of 34 patients with Parkinson's disease from the time of initiation of drug treatment explored changes in the motor response to L-dopa over the early to mid disease course. Motor fluctuations developed in 41% after a mean L-dopa treatment interval of 25 months and dyskinesia developed in 53% after a mean of 15 months' treatment. Patients who developed fluctuations had a significantly better response to L-dopa than nonfluctuators. Nonfluctuators also had significantly greater "midline" motor disability affecting cranial and truncal muscles and gait. The development of motor fluctuations may simply reflect a retained capacity to respond to L-dopa as endogenous dopaminergic neurotransmission declines with progressive nigral cell loss. Many patients who show no sign of motor fluctuation 5 or 6 years into the disease course have a relatively blunted response to L-dopa. The proportion of such cases seems to correspond to the percentage that have coexisting striatal pathologic changes in postmortem studies.

How long should a routine EEG be?

Cost-benefit analysis in neurology practice deserves continual reassessment. One example is the duration of a routine electroencephalography (EEG) required to optimise accuracy of diagnosis. Recommended guidelines of recording a routine EEG for 20 or more minutes are not based on scientific evidence. In many countries, EEG is not economically viable with costs outweighing financial remuneration. We prospectively studied 420 consecutive routine EEGs to see if a shorter record decreased diagnostic accuracy. A carefully structured 15 min routine EEG protocol produced comparable results with the 25 min recording. Shorter routine EEGs would make EEG more cost effective without compromising diagnostic accuracy.