[Parkinsonism during lithium use]. / Parkinsonisme bij lithiumgebruik.

Two patients with bipolar disorder had been treated for years with lithium without any complications but began to develop symptoms of rigidity and an altered gait, namely symptoms compatible with a diagnosis of Parkinsonism with an action tremor. In both patients lithium levels were within the therapeutic range. Medication-induced Parkinsonism occurs frequently in patients using antipsychotic medication, but is a rare complication in patients receiving long term treatment with lithium. The lithium dosage was reduced gradually and within a few months all neurological symptoms subsided completely.

[Transient global amnesia: indications for a syndrome involving cerebral venous stasis]. / Voorbijgaand geheugenverlies ('transient global amnesia'): aanwijzingen voor een syndroom van cerebrale veneuze stase.

In 3 patients, a woman aged 58 and 2 men aged 61 and 58, respectively, who presented to the Emergency Clinic with sudden antegrade and retrograde amnesia, the diagnosis 'transient global amnesia' (TGA) was made. In the first and the last patient the TGA was preceded by a Valsalva-like manoeuvre, i.e. vomiting and tying the shoelaces while bending over and holding his breath, respectively. Until recently, TGA was assumed to have three possible causes: arterial ischaemia (transient ischaemic attack; TIA), migraine and epilepsy. A fourth and more recent hypothesis is cerebral venous stasis. This is in accord with the haemodynamic changes that have been described as a provoking factor in TGA. A Valsalva-like manoeuvre increases the intrathoracic pressure, followed by venous reflux in the internal jugular vein. The resultant cerebral venous congestion can cause temporary ischaemia of mesiotemporal structures, such as the hippocampus, and lead to transient cerebral dysfunction. Recent studies support this haemodynamic pathogenesis. The aetiology of TGA is probably multifactorial, with cerebral venous stasis probably playing an important role. There is still no good explanation for the observation that a causative factor usually leads to a TGA in the same person only once.

Transthoracic echo/Doppler in the identification of patients with chronic non-valvular atrial fibrillation at risk for thromboembolic events.

UNLABELLED: Left atrial spontaneous echo contrast, detected by transoesophageal echocardiography in patients with non-valvular atrial fibrillation reflects slow blood flow and is associated with an increased risk of cardio-embolism. The purpose of this study was to find echo/Doppler predictors of left atrial spontaneous echo contrast by transthoracic examination. In a retrospective case control study, 17 patients with chronic non-valvular atrial fibrillation who had suffered a recent cerebral ischaemic event (group A) and 17 patients with chronic non-valvular atrial fibrillation who had not suffered such an event (group B) were studied. Both groups were matched for age and sex. All patients underwent standard transthoracic echocardiography with transmitral Doppler as well as transoesophageal echocardiography. Left atrial spontaneous echo contrast was demonstrated by transoesophageal echocardiography in nine group A patients and in two group B patients (P = 0.028); left atrial spontaneous echo contrast was not detected by transthoracic echocardiography in these patients. All patients with left atrial spontaneous echo contrast (11 patients) had a left atrial size, corrected for base index, exceeding 24 mm and a transmitral time velocity integral < 10 cm (sensitivity 100%). Left atrial spontaneous echo contrast was absent in six patients with both characteristics (specificity 74%). CONCLUSION: transthoracic echo/Doppler aids in the prediction of the presence of left atrial spontaneous echo contrast and the identification of patients with non-valvular atrial fibrillation with increased cardioembolic risk, thus avoiding transoesophageal echocardiography.

TIA, RIND, minor stroke: a continuum, or different subgroups? Dutch TIA Study Group.

The results of CT were studied prospectively in 606 patients with a transient ischaemic attack (TIA), 422 patients with a reversible ischaemic neurological deficit (RIND), and 1054 patients with a minor stroke, were all entered into a multi-centre clinical trial. CT scanning showed a relevant ischaemic lesion in 13% (95% confidence interval 10-16%) of TIAs, 35% (95% confidence interval 30-40%) of RINDs, and 49% (95% confidence interval 46-52%) of minor strokes (p less than 0.000001). Even within the 24 hour margin, relevant infarcts occurred more often with longer attacks, but were still found in some patients with attacks lasting less than a minute. The type and location of the infarcts were similar in the three groups. These findings suggest that the differences between TIAs, RINDs, and minor strokes are quantitative rather than qualitative.

Transient ischemic attacks with and without a relevant infarct on computed tomographic scans cannot be distinguished clinically. Dutch Transient Ischemic Attack Study Group.

We prospectively studied clinical and computed tomographic (CT) scan findings in 79 patients with a transient ischemic attack (TIA) and a relevant cerebral infarction on CT, also known as cerebral infarction with transient signs (CITS). We compared the results with those of 527 concurrent patients with TIA and without cerebral infarction and also with 646 patients with persistent neurological symptoms and a relevant infarct on CT. All patients were participating in a multicenter trial. In both groups, most infarcts were of the lacunar type. Compared with TIAs without cerebral infarction, patients with CITS slightly more often had a history of hypertension (52% vs 33%), the attacks lasted longer (greater than 1 hour, 52% vs 34%) and disappeared more slowly (over the course of hours, 39% vs 24%), and the symptoms more frequently involved speech (61% vs 41%). Despite these small differences, the reverse--the prediction of evidence on CT of infarction on the basis of the nature or time course of symptoms--proved impossible, since in each category the majority of patients had a normal CT scan. In comparison with patients with stroke and visible infarction, patients with CITS slightly more often had abnormal speech (61% vs 45%) and had a larger number of attacks (multiple attacks, 46% vs 18%). In conclusion, we found only minor clinical differences between patients with TIA with or without a relevant infarct on CT and equally small differences between patients with CITS and patients with stroke and cerebral infarction. These clinical similarities do not exclude a difference in prognosis.

Spatial contrast sensitivity in unilateral cerebral ischaemic lesions involving the posterior visual pathway.

Contrast sensitivity function was studied in 16 patients with unilateral ischaemic lesions involving the posterior visual pathway. Sixty-two percent of the patients showed contrast sensitivity loss in at least one eye for horizontal or vertical stimulus orientation. Visual perception was distorted in a qualitatively different way according to the anteroposterior site of the lesion. Patients with occipital or occipitotemporal lesions showed high spatial frequency selective losses and patients with temporal or parietal lesions low frequency selective losses. Stimulus orientation selectivity was observed in patients with lesions of the primary visual cortex as well as in patients with lesions anterior to the striate cortex. Contrast sensitivity orientation-selective losses were demonstrated in 14 of the 17 'affected' eyes.

Visual contrast sensitivity in drug-induced Parkinsonism.

The influence of stimulus orientation on contrast sensitivity function was studied in 10 patients with drug-induced Parkinsonism. Nine of the 10 patients had at least one eye with contrast sensitivity deficit for vertical and/or horizontal stimuli. Only generalised contrast sensitivity loss, observed in two eyes, was stimulus orientation independent. All spatial frequency-selective contrast deficits in 15 eyes were orientation dependent. The striking similarity between the pattern of contrast sensitivity loss in drug-induced Parkinsonism and that in idiopathic Parkinson's disease, suggests that generalised dopaminergic deficiency, from whatever cause, affects visual function in an analogous way.

Spatial contrast sensitivity in benign intracranial hypertension.

Spatial Contrast Sensitivity (CS) was studied in 20 patients with benign intracranial hypertension (BIH). At presentation CS loss was found in 43% of the eyes, and impairment of visual acuity attributed to BIH in only 16%. Nine patients had blurred vision or visual obscurations, all of whom had abnormal CS. The clinical application of CS measurement in BIH for monitoring the progression or regression of the disease is illustrated by serial measurements in 11 patients. Progressive visual loss in longstanding papilloedema and improvement of visual function in subsiding papilloedema can occur without any change in Snellen acuity or visual field charting.

Effect of stimulus orientation on contrast sensitivity in Parkinson's disease.

We studied the effect of stimulus orientation on contrast sensitivity function in 21 patients with Parkinson's disease and in 10 normal subjects. This was done by measuring contrast sensitivity over a range of spatial frequencies for vertical and horizontal sine wave grating stimuli. There was a great test-retest consistency in normal subjects and patients. Fifteen of the 21 patients showed contrast sensitivity deficit in at least one eye. Orientation-specific loss was demonstrated in 17 of the 25 "affected" eyes. The most frequent type of orientation-specific loss was a notch defect, which preferentially affected the middle spatial frequencies. We attribute orientation-specific and spatial frequency-selective loss in Parkinson's disease to a functional disruption of neurons on the visual cortex.

Spatial contrast sensitivity in clinical neurology.

We studied contrast sensitivity function in normal subjects and in three illustrative cases with various neurological disorders. This was done by measuring contrast sensitivity over a range of spatial frequencies for vertical sinewave grating stimuli. It is demonstrated that contrast sensitivity function can give information about visual function not obtainable by conventional test procedures.

Effect of levodopa treatment on contrast sensitivity in Parkinson's disease.

We studied contrast sensitivity function in 10 parkinsonian patients before and after levodopa treatment. Pretreatment contrast sensitivity function was abnormal in 16 of the 20 eyes. After treatment, only high-frequency loss was observed in 6 eyes. All other types of deficit disappeared under treatment. These changes of contrast sensitivity function following treatment suggest that dopamine is a functional transmitter in the visual pathways.

Contrast sensitivity in Parkinson's disease.

We studied contrast-sensitivity function in 39 patients with Parkinson's disease. Sixty-four percent of the patients showed contrast-sensitivity loss in one or both eyes. The abnormality was not related to the first symptom or the severity of disease. Sensitivity loss at intermediate frequencies (notch loss) in 30% of the "affected" eyes suggested a cortical component. These findings support the belief that there is a widespread neurotransmitter deficiency in Parkinson's disease.

Benign intracranial hypertension. A retrospective and follow-up study.

Thirty-six patients with benign intracranial hypertension (BIH) were reviewed. Follow-up was obtained on 33 patients (91%) after a mean period of 7 1/2 years. Precipitating factors were found in 27 patients (75%). On admission, 5 patients had retro-ocular pain, especially on eye movements, a complaint not yet described in BIH. Seven patients had nystagmus, two of them horizontal positional nystagmus. It is questionable whether all signs in BIH are caused by the raised CSF pressure. The general outcome was good. Only two patients sustained severe ultimate visual impairment. Both presented with retro-ocular pain and sudden loss of vision on admission. Papilloedema can persist for years in BIH without serious visual impairment. Sometimes "causal" treatment is possible. No symptomatic treatment which is free from complications has been proved to prevent visual failure.