Open-labelled observations of language dysfunction in old ischemic stroke patients with aphasia when given plant and marine-based nutrient supplements for 12 weeks.

BACKGROUND AND OBJECTIVES: This study aimed to explore the effect of functional foods on aphasia related to a previous ischemic stroke. When stroke-related neurological deficits result in physical dependency and poor selfcare that persists longer than 6 months, full recovery is almost impossible and the patient often requires long-term care. The functional foods, EASE123 and BioBalance#6, include numerous plant and marine-based nutrient supplements that could prove beneficial for such patients. METHODS AND STUDY DESIGN: This open-labelled study included 10 patients diagnosed with prior ischemic stroke and aphasia lasting longer than 6 months. Each patient was administered 6 tablets of EASE123 at 10:30 AM and at 90 minutes before sleeping, and 3 tablets of BioBalance# 6 at 2:30 PM. After a treatment period of 12 weeks, the patients were followed during a 4-week withdrawal period. Functional improvement was assessed by scores and subscores on the Concise Chinese Aphasia Test (CCAT) at weeks 4, 8, 12, and 16. RESULTS: Average total CCAT scores and matching ability improved significantly at weeks 4, 8, 12, and 16 (p<0.05). Simple response scores improved significantly at weeks 8 and 12 (p<0.05). Auditory comprehension improved significantly at weeks 4 and 12 (p<0.05), and reading comprehension, at week 12 (p<0.05). Repetition ability improved significantly at weeks 8, 12, and 16 (p<0.05), and spontaneous writing, at weeks 4, 12, and 16 (p<0.05). CONCLUSIONS: Matching, repetition, and average total CCAT scores improved over the course of the study. Therefore, 6 months after ischemic stroke, EASE123 and BioBalance# 6 administration may improve stroke-related aphasia.

Vertebral artery injury presenting with signs of middle cerebral artery occlusion. A case report.

Therapeutic manipulation of the neck has been shown to produced injury to the vertebral artery. The clinical syndromes produced by this arterial insufficiency generally reflect dysfunction of the brainstem or cerebellum. The authors present a case of such injury that presented with clinical findings, namely, hemiparesis and aphasia, suggestive of involvement of the dominant middle cerebral artery. These findings may have been the result of disruption of flow through the posterior cerebral artery to the thalamus, internal capsule, and cerebral peduncles.

Interaction between psychological and pharmacological treatment in cognitive impairment.

In contrast to other kinds of psychotropic drugs, nootropics or cognition enhancing drugs may be indicated, not for the direct treatment of the pathology itself, but for improving or restoring the remaining brain functions. Brain functions are normally trained during various kinds of non-medical therapy, such as physiotherapy, speech therapy, occupational therapy, memory training etc... In research little attention has been paid to the combination of both kinds of therapeutic approaches, probably because of the important methodological difficulties. This combination however, offers various interesting perspectives: L. ISRAEL examined in two placebo-controlled studies the effects of either 160 mg/d of ginkgo biloba extractum (GBE) or piracetam 2.4 or 4.8 g/d, combined with a memory training program, in nondemented patients complaining of memory problems. The results of both studies suggest that nootropic drug treatment and memory training have each an effect on different cognitive functions and, hence, are complementary. Some functions, like attention/perception in the GBE study and learning in the piracetam study, seem to benefit from both treatments, suggesting a mutually potentiating effect of drug treatment and training. This potentiation is very clear in the treatment of dyslexic children: in a placebo-controlled study piracetam 3.3 g/d, in combination with normal school teaching and more specific logopedic therapy, allowed a normal progression during the full school year in reading accuracy and reading comprehension, while the placebo treated children getting a similar training progressed only with 50%. Recently promising results were obtained in the treatment of dysphasic patients with a combination of speech therapy and piracetam 4.8 g/d, especially when given during the first months after the stroke, or otherwise in combination with an intensive speech training. In both double-blind studies the piracetam treated group improved about 60% more than the group who only got speech therapy and placebo. All these data may be explained by the restorative or enhancing influence of nootropic drugs on neurotransmitter systems closely related to learning and memory functions. E.g. piracetam restores the availability and function of muscarinic and NMDA receptors in aging animals, most probably through a modulation of the psychico-chemical properties of the neuronal membrane such as the membrane fluidity.

Is cerebral arteritis the cause of the Landau-Kleffner syndrome? Four cases in childhood with angiographic study.

Four children with Landau-Kleffner syndrome were studied over a six year period. They presented with acquired aphasia, epilepsy, and focal or generalized EEG discharges which were exacerbated during sleep. In addition, cerebral angiography demonstrated isolated arteritis of some branches of the carotid arteries in all cases. Computed tomographic and magnetic resonance images were normal. Nicardipine in a dose of 1 to 2 mg/kg/day, added to conventional anticonvulsant drugs provided effective supplementary control of seizures, of paroxysmal EEG discharges, and of language and behavioural disturbances, even several years after the onset of the disorder and in patients whose response to other medications, including steroids, had been poor. Interruption of nicardipine administration was followed by relapse of the language disorder. Repeat angiography was performed in all four patients and showed recanalization of obstructed vessels in two cases. Focal cerebral vasculitis may be the pathogenesis of the Landau-Kleffner syndrome and calcium channel blockers such as nicardipine may be effective and specific therapy.