Ottar Sjaastad

Clonazepam (rivotril) in migraine prophylaxis.

SYNOPSIS

WHIPLASH: CHRONIC ORGANIC BRAIN SYNDROME WITHOUT HYDROCEPHALUS EX VACUO

Eleven patients who had sustained whiplash injuries to the neck were studied by pneumo‐encephalography, by a variety of psychological tests, and by psychiatric evaluation with a view to assessing whether organic CNS changes might, in some cases, be a consequence of such injuries. Patients with traumatic encephalopathy, and age‐ and sex‐matched groups of patients served as control groups. Pneumo‐encephalography showed normal findings in the whiplash group as a whole, the width of the ventricular system being significantly smaller than that of patients with traumatic encephalopathy. Psychological tests and psychiatric evaluation indicated that organic brain pathology was present in the whiplash patients, although to a lesser extent than in patients with traumatic encephalopathy.

THE SIGNIFICANCE OF BLOOD SEROTONIN LEVELS IN MIGRAINE A Critical Review

Available evidence indicates that serotonin located within platelets—or lack of it—does not precipitate migraine attacks, and that intravenously administered serotonin is beneficial in migraine. On this premise, it is not likely that the beneficial effect of intravenously administered serotonin is due to replacement of lost intracellular serotonin. If serotonin is effective in relieving migraine pain, this is probably due to extracellular serotonin acting on the cardiovascular system. In other words, serotonin‐induced relief in migraine is probably caused by the pharmacological properties of the amine—it probably acts as a drug and not by replacement. The serotonin changes in migraine are probably not primary, but caused by the disease process. Platelets may nevertheless be of importance in the pathogenesis of migraine, and serotonin may be of even more interest. However, interest in platelet serotonin will probably be diminishing in the future.

2‐(2.6‐DICHLOROPHENYLAMINO)‐2‐IMIDAZOLINE HYDROCHLORIDE (ST 155 OR CATAPRESAN) AS A PROPHYLACTIC REMEDY AGAINST MIGRAINE

Twenty‐six migraine patients were included in a double blind study of the migraine‐reducing effect of 2‐(2.6‐dichlorophenylamino)‐2‐imidazoline hydrochloride (ST 155 or Catapresan). Sixteen of 26 patients (i.e. 62 per cent) experienced a reduction in headache indices when medicated with 75 μg of ST 155 daily (p < 0.025). The side effects of ST 155 in this dosage were trifling: a few patients complained of slight thirst, dryness of the mouth, or slight lethargy during the initial phase of drug therapy.

INTESTINAL ABSORPTION IN MYOTONIC DYSTROPHY

Forty‐four patients with myotonic dystrophy were subjected to various tests for intestinal absorption. A varying number of patients were subjected to the various tests. In one patient (of altogether 11 patients) a pathological vitamin A absorption test was found together with increased faecal excretion of fat and nitrogen. Two of 12 patients showed pathological D‐xylose tests. The reason for this may possibly be deficient urine collection. Schilling tests were one the whole normal. Glucose tolerance tests were pathological in 26 of 35 patients. The following pathological findings were made: elevated fasting blood sugar, elevated peak level, delayed return to pretest level, biphasic response and reduced increment in blood glucose levels following loading. The biphasic response seems to be a rather characteristic finding in myotonic dystrophy. The peak concentration was in all except one case reached within 15–60 minutes. Intravenous glucose loading gave normal response curves. The pathological response on oral loading was probably often caused by intestinal motility disturbances and not by malabsorption. Malabsorption seems to be a rare feature of myotonic dystrophy.

THE CORPUS CALLOSAL ANGLE IN THE DIAGNOSIS OF CEREBRAL VENTRICULAR ENLARGEMENT

The corpus callosal angle was measured in 5 groups of patients: control patients, patients with hydrocephalus ex vacuo, patients with normal pressure hydrocephalus, patients with probable normal hydrocephalus and patients with pressure hydrocephalus. The diagnosis of normal pressure hydrocephalus was based on isotope cisternography and the failure of air to accumulate on the surface near the sagittal sinus during airencephalography. The angle in controls (mean 134°) and patients with hydrocephalus ex vacuo (mean 135°) was almost invariably ≧ 120°, and was significantly different from the mean angle in the pressure hydrocephalus group (105°) (P<0.001). The mean angle in the normal pressure hydrocephalus group (118°) was significantly lower than the angle in the hydrocephalus ex vacuo group (P <0.01). There was some overlap between the angles in these two groups. An angle below 120° usually indicates pressure or normal pressure hydrocephalus. On the other hand, an angle exceeding 120° is compatible with both pressure and normal pressure hydrocephalus as well as hydrocephalus ex vacuo.

Increased Intracranial Pressure in So-Called ‘Normal-Pressure Hydrocephalus’

Five patients exhibited an apparently communicating hydrocephalus -- type of disorder, with ventricular reflux on the cisternograms, lack of air-encephalographic parasagittal air-filling and clearly enlarged temporal horns. The group seemed heterogeneous, with regard to age distribution; possible etiological factors and duration of the hydrocephalic process. In all 5 patients increased intracranial/intrathecal pressure was observed: in 2 patients, only with intrathecal measurement in the lumbar area, but in the remaining 3 patients with epidural/ventricular fluid pressure monitoring. Continuously increased pressure extending over 1 or more days was observed in these patients. This pressure increase may seem different from the episodic pressure increase previously reported in normal-pressure hydrocephalus. These patients seem to be cases of so-called normal-pressure hydrocephalus according to the commonly accepted criteria. It is therefore suggested that the term normal-pressure hydrocephalus should be abandoned, and replaced by, e.g., low-pressure hydrocephalus, malresorptive or malabsorptive hydrocephalus.

PNEUMOENCEPHALOGRAPHIC FINDINGS IN VARIOUS PRIMARY and SECONDARY MUSCULAR DISORDERS

Pneumoencephalography was carried out in 23 patients with various muscular disorders, i.e. spinal neurogenic atrophy, classified as Wohifart‐Kugelberg‐Welanders and Charcot‐Marie‐Tooths diseases, and muscular dystrophy. EEG‐registrations and psychological testing were carried out. Pneumoencephalography revealed ventricular enlargement and cortical changes in 17 out of 23 cases. Changes were found in all three groups studied; cortical changes were, however, only found in the neurogenic atrophy groups. Cases where there clearly might be exogenous causes for ventricular dilatation were excluded. the changes found, therefore, supposedly form an integral part of the disease process. It should be emphasized that the precaution does not entirely exclude a traumatic etiology in some cases. EEG‐registrations (pathological in three out of 20 cases) as well as psychological evaluation (pathological in six out of 14 cases) supported the assumption of organic brain changes. Pneumoencephalography, however, seemed to be the most sensitive parameter for unveiling brain involvement in these disorrders.

Cellular transport of l-histidine in Hartnup disease

The urinary excretion, the intestinal absorption, and the elimination of histidine from blood were studied in two patients with Hartnup disease. On standard diet the patients lost a great proportion of the dietary histidine in the urine, whereas the fecal loss was negligible. A high oral dose of L-histidine gave only a slight increase in plasma histidine and no increase in fecal histidine, but a considerable increase in the urinary histidine output. Intravenously administered L-histidine was eliminated more rapidly than in controls. The lack of increase in plasma histidine after the oral loading may be explained by the rapid elimination from the blood. This was mainly due to a rapid cellular uptake of histidine which is supposed to be a normal reaction of histidine-deprived cells. Thus the only obvious defect in the histidine transport in Hartnup disease is the reabsorption defect in the renal tubules. A generally impaired cellular transport of L-histidine is improbable.

Histaminuria in Hartnup disease.

Two patients with Hartnup disease showed increased urinary excretion of conjugated histamine and increased faecal excretion of histamine‐like activity. After addition of L‐histidine, histamine was formed in faecal specimens in vitro. After ingestion of L‐histidine there were signs of no more than a moderate intraluminal formation of histamine in the large bowel. These findings indicate that in Hartnup disease there is no marked malabsorption of L‐histidine, a thesis that will be tested further.