Trilochan Srivastava

Fungal granuloma of the brain caused by Cladosporium bantianum--a case report and review of literature.

Involvement of the brain by neurotropic, dematiaceous fungi namely Cladosporium bantianum is extremely rare. The disease is very resistant to treatment and prone for frequent relapses despite treatment with amphotericin B and flucytosine, the drugs of choice for the infection. Surgery is often required for resection of the fungal granuloma. Isolation of the fungus from the tissue specimens and its culture, showing dark colored fungal colonies clinches the diagnosis. Animal inoculation studies can provide insights to the portal of entry of the organism. We hereby report a case of fungal granuloma of the brain due to C. bantianum, which responded favorably to intensive antifungal treatment alone, with relevant review of literature.

Limb-Shaking Transient Ischemic Attack Induced by Middle Cerebral Artery Stenosis

421 Dr. V. Puetz, Department of Neurology Technical University Dresden, Fetscherstrasse 74 DE–01307 Dresden (Germany) Tel. +49 351 458 3565, Fax +49 351 458 4365 E-Mail volker.puetz@neuro.med.tu-dresden.de 9 Hacke W, Albers G, Al-Rawi Y, Bogousslavsky J, Davalos A, Eliasziw M, Fischer M, Furlan A, Kaste M, Lees KR, Soehngen M, Warach S; DIAS Study Group: The Desmoteplase in Acute Ischemic Stroke Trial (DIAS): a phase II MRI-based 9-hour window acute stroke thrombolysis trial with intravenous desmoteplase. Stroke 2005; 36: 66–73. 10 Abciximab in acute ischemic stroke: a randomized, double-blind, placebocontrolled, dose escalation study. The Abciximab in Ischemic Stroke Investigators. Stroke 2000; 31: 601–609. 11 Lapchak PA, Araujo DM: Therapeutic potential of platelet glyocoprotein IIb/IIIa receptor antagonists in the management of ischemic stroke. Am J Cardiovasc Drugs 2003; 3: 87–94. 12 Selim M, Kumar S, Fink J, Schlaug G, Caplan LR, Linfante I: Seizure at stroke onset: should it be an absolute contraindication to thrombolysis? Cerebrovasc Dis 2002; 14: 54–57. 13 Yasaka M, Yamaguchi T, Yonehara T, Moriyasu H: Recurrent embolization during intravenous administration of tissue plasminogen activator in acute ischemic stroke. A case report. Angiology 1994; 45: 481–484. 14 Bautista RED: Embolic stroke following thrombolytic therapy for myocardial infarction in a patient with preexisting ventricular thrombi. Stroke 1995; 26: 324–325. 15 Derex L, Nighoghossian N, Perinetti M, Honnorat J, Trouillas P: Thrombolytic therapy in acute ischemic stroke patients with cardiac thrombus. Neurology 2001; 57: 2122–2125.

A study of voice profiles and acoustic signs in patients with Parkinson’s disease in North India

We aimed to study the voice profiles of patients with Parkinsons disease (PD) and correlate the profiles with disease severity. A total of 133 patients with PD were recruited. Patients were divided into two groups: Group 1 with a Unified Parkinsons Disease Rating Scale (UPDRS) score of ≤45; and Group 2 with a UPDRS >45. Speech was analyzed using the Indian Speech and Hearing Association (ISHA) articulation assessment and Vaghmi software. A total of 87 patients (65.41%) reported a history of speech problems. Examination revealed slow reading speed (64.7% of patients), hoarseness of voice (60.2%), articulatory defect (39.8%) and jerky speech (32.3%) as common abnormalities. Misarticulation was most often observed among the labial (42.1%), followed by lingual and palatal syllables. The ISHA articulation test demonstrated significant differences in mean numbers of words distorted (p<0.001) and intelligible speech (p=0.004) between patients with early and advanced PD. Vaghmi software analysis (Speech and Voice Systems, Bangalore, India) also revealed significant difference between the two groups in maximum phonation duration (p=0.034), inability to phonate (noiseless speech, Z; p=0.002) and the mean noise-to-noiseless speech (S/Z) ratio (p=0.006).

Hemichorea-hemiballism associated with frontoparietal bleed

Sirs: We report a case of hemichorea-hemiballism involving the left upper limb following a frontoparietal bleed. Hemichoreahemiballism associated with a fronto-parietal lobe bleed has not previously been described in the literature. A 53-year-old woman presented with sudden onset of involuntary movements of her left upper limb. There were flinging, violent and arrhythmic movements, occurring several times a minute. After 5–7 days, these violent movements subsided in intensity and were replaced by forcible, jerky, dancinglike movement suggestive of choreiform movements. There was no past history of stroke, coronary artery disease, hypertension or diabetes mellitus. Her vital signs were normal including blood pressure. The patient was alert. Cranial nerves including fundus examination were normal. There were no cerebellar signs. Motor power, deep tendon jerks and sensory (primary and cortical) examination were also normal. Non contrast enhanced CT revealed a right frontoparietal hemorrhage with mild edema. No mass effect or midline shift were present (Fig. 1). Since the patient was normotensive with an unusual site of her intracranial bleed, search was made for a cause of hemorrhage. The hemogram, bleeding time, clotting time, prothrombin time and platelet counts were normal. Renal and liver function tests were also normal. Lupus anticoagulant, antiphospholipid antibody and antinuclear antibody were negative. MRI confirmed the presence of hematoma without any evidence of involvement of subthalamus, thalamus or basal ganglia. Digital subtraction angiography (DSA) for cerebral vessels was normal. There was no evidence of venous sinus thrombosis. The patient was managed conservatively and gradually hemiballism resolved within a week and hemichorea appeared which subsided in the next 2 weeks. Although hemichorea-hemiballism is usually linked to a lesion in the subthalamus, in this case subthalamus, thalamus and basal ganglia were normal and the only lesion was present in the frontoparietal lobe. Hemichoreahemiballism due to parietal lobe involvement has been described, but it is extremely rare [3, 5]. Mizushima et al. described a case of hemichorea-hemiballism associated with parietal lobe infarction [4]. In another case hemiballismhemichorea developed post-operatively in a 28-year-old man with meningioma in his right parasagittal parietal lobe [6]. CT immediately after surgery revealed a small hematoma in the tumor bed without any additional lesion in thalamus or basal ganglion. A pure cortical infarction sparing the basal ganglion seldom produces hemichorea-hemiballism. Schwarz and Barrows speculated that interruption of neural circuits from some part of the frontal or parietal cortex to caudate nucleus and putamen as the possible mechanism for hemiballism [5]. Hemiballism following left frontal lobe infarction was reported by Martin who suggested that ischemia of a cerebral hemisphere affected the basal ganglion and hence produced hemiballism [3]. An extensive literature search did not show hemichorea-hemiballism due to fronto-parietal lobe bleed. It has been suggested that a lesion of the subthalamic nucleus (STN) reduces striato-pallidal inhibitory influences leading to reduced excitory projections from the STN to pars interna of globus pallidus, which in turn disinhibits thalamus and cortex resulting in hyperkinetic movements [1]. The somatosensory cortex also projects to the putamen and may influence this basal ganglion circuit [2]. It is believed that the parietal lobe, especially Brodmann’s area 7, may be one of the areas inducing hemiballism [6]. We propose that these abnormal movements may occur if the basal ganglion-thalamo-cortical circuit is affected anywhere, as in this case it was in the fronto-parietal lobe.