Central pontine myelinolysis, an update.

Central pontine myelinolysis (CPM) can be regarded as one of the demyelinating syndromes. First described by Adams et al. in 1959 in their chronic alcoholic patients, it has now been described in the malnourished, the chronically debilitated, the renal, the hepatic and the transplant patient among others. Pathologically, it is defined as a symmetric area of myelin disruption in the center of the basis pontis, although similar symmetric lesions have also been described occurring with CPM as well as independently in other brain areas (extrapontine myelinolysis or EPM) including the cerebellar and neocortical white/gray junctional areas, thalamus and striatum. Possible mechanisms include a hyperosmotically induced demyelination process resulting from rapid intracellular/ extracellular to intravascular water shifts producing relative glial dehydration and myelin degradation and/or oligodendroglial apoptosis. The process most often occurs during rapid rebalancing of the electrolyte parameters in the hyponatremic patient. Avoidance of CPM/EPM is dependent upon recognizing those patients with conditions pre-disposing them to osmotic myelinolysis and then moderating the rate of normalization of the electrolyte imbalance. The morbidity and mortality of CPM/EPM has been greatly reduced by recognition of pre-disposing conditions, increased understanding of the pathophysiology, intensive treatment, and rapid diagnosis and monitoring with advanced neuroimaging.

An occipital lobe epileptogenic focus in a patient with West Nile encephalitis.

Although most human cases of West Nile (WN) fever are benign, approximately 1% produce severe neurological illness. Meningitis and/or encephalitis comprise 75% of hospitalized cases with seizures in 10-15%. Occipital lobe seizures, often mimicking other primary seizure types due to extra-occipital spread, is uncommon in adults and especially so from an infectious origin. A case of WN encephalitis presenting with a simple partial seizure, focal motor, resulting from an occipital epileptogenic focus is reported. The atypical epileptogenic location of the case and the observed frequency of seizures in WN encephalitis suggest that this virus is particularly irritative to cortical neuronal networks. Thus when seizures especially with atypical EEG patterns present during an acute febrile illness in the warmer months, WN encephalitis should be considered.

False aneurysm of the common femoral artery after total hip arthroplasty. A case report.

A 59-year-old healthy man presented with osteoarthritis of his left hip that was recalcitrant to nonoperative treatment. He subsequently elected to have arthroplasty of the hip performed. At 3 months after arthroplasty, he returned reporting progressive groin pain: most remarkable was a palpable mass in the groin region. An arteriogram showed a radiodense mass adjacent to the acetabulum, and a computed tomography scan with contrast confirmed a large false aneurysm originating from the common femoral artery. In this particular case, a pointed Hohmann retractor punctured the common femoral artery, creating the dynamics of the development of a false aneurysm. Primary suture repair of the vascular defect was performed, followed by a complete and uncomplicated recovery of the patient to full activity. Since this case, the authors have discontinued the use of pointed. Hohmann retractors and now use a blunt, rounded Hohmann retractor during total hip arthroplasty without compromising acetabular exposure. However, care must be taken in blunt retractor placement to avoid retractor slippage during the procedure. This case shows the need for awareness of potential mechanisms for vascular injury related to total hip arthroplasty.

Preventing relapse. Guidelines for the pediatrician.

Preventing relapse into substance use means first helping the teenager to develop a state of recovery. This involves completing a First Step of a 12-Step program, whereby the teenager accepts that drugs and alcohol have been destructive in his or her life and that moderate use is impossible. Thus, abstinence is necessary in a productive life. Parental support is also established. The two more common causes of relapse are being in the presence of alcohol- and drug-using peers and the presence of co-existing psychiatric problems.

Intranasal abuse of prescribed methylphenidate by an alcohol and drug abusing adolescent with ADHD.

A rare case is described where an adolescent with attention deficit hyperactivity disorder diagnosed in childhood subsequently developed alcohol and drug abuse. He later developed intranasal methylphenidate abuse and dependence after realizing that urine drug screens were expected to be positive for prescribed methylphenidate. This report is to alert physicians to the rare possibility of intranasal methylphenidate abuse in chemically dependent teenagers treated for ADHD and also to the possibility of group methylphenidate abuse at special education schools where many teenagers may be treated with stimulant medication.

Methylphenidate and hospitalized adolescents with conduct disorder: Dose effects on classroom behavior, academic performance, and impulsivity.

The effects of methylphenidate on hospitalized conduct-disordered (CD) adolescents were examined by using teacher ratings of behavior, a measure of classroom learning, and a test of impulsivity. Twenty-two male adolescents with CD, 12-18 years of age, participated in a double-blind, placebo-controlled, within-subject (crossover) design in which each adolescent received three doses of methylphenidate (10 mg, 15 mg, and 20 mg) and a placebo in a randomly assigned, counterbalanced order. Seven of the adolescents had a comorbid diagnosis of attention deficit hyperactivity disorder. Significant overall medication effects were shown on teacher ratings of conduct, and on number of arithmetic questions correctly completed and time spent. Within the limitations of this study, stimulant actions may be effective for some aspects of CD in the absence of attention deficit hyperactivity disorder, although only for specific measures.

The startle response in rats: effect of ethanol.

The effects of acute and chronic ethanol intake on the startle response was examined in male rats. Ethanol given IP produced a dose-dependent decrease in the amplitude of the startle response measured 30 min later. With a dose of 1 g/kg, the effect was evident at 15 min and had recovered substantially by 60 min. The effect of ethanol on the startle response was potentiated by pretreatment of the animals with pimozide, haloperidol, and p-chlorophenylalanine but not by propranolol, phenoxybenzamine, alpha-methyltyrosine, or pargyline. After 3 weeks on an ethanol-containing diet, the startle response was greater than that shown by rats on the control iso-caloric, sucrose-containing diet. After ethanol withdrawal, the startle response was further increased, with a peak about 9 to 12 hr after discontinuation of ethanol; thereafter, the response declined. This time course of heightened startle response during ethanol withdrawal corresponds to the time course of the activation of noradrenergic neurons during withdrawal. It appears that dopaminergic and serotonergic neurons are involved in the mediation of the startle response in rats.