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Biomedical subjects

N Giladi

Publications and source records attributed to N Giladi.

At least 73 records · Page 4Linked to original sources
PubMed1997

Freezing phenomenon in patients with parkinsonian syndromes.

Freezing is a common symptom in parkinsonian syndromes, but its association with different causes of parkinsonism as well as with other symptoms has never been investigated. We conducted a database survey of the occurrence of freezing in parkinsonism. Of 347 patients with a clinical diagnosis of parkinsonism other than idiopathic Parkinson's disease and with specific data regarding freezing, 158 patients had freezing (46%). Freezing was significantly associated with progression of the disease as rated on the Hoehn & Yahr scale [odds ratio (OR), 1.69; p < 0.004]. Gender was not a risk factor for the development of freezing. Patients with drug-induced parkinsonism were at a very low risk for developing freezing (p < 0.00001; OR, 0.1). Freezing was found in a high frequency in patients with vascular parkinsonism (57%), normal-pressure hydrocephalus (56%), and generally in the group of patients who had parkinsonism resulting from neurodegenerative diseases (progressive supranuclear palsy, multiple system atrophy, and corticobasal ganglionic degeneration; 45%). Freezing was significantly associated with the presence of dementia, incontinence, and tachyphemia (OR, 2.01, 1.7, and 5.09, respectively).

Dementia↗
PubMed1997

Globus pallidus internus pallidotomy for generalized dystonia.

The authors present a young boy with severe generalized dystonia treated with bilateral simultaneous pallidotomy. Microelectrode recordings with the patient under propofol anesthesia showed that the mean discharge rate of globus pallidus internus (GPi) neurons was between 21 and 31 Hz. This contrasts sharply with the mean GPi neuronal firing rates of approximately 80 Hz that are characteristic of Parkinson's disease. The patient had no immediate benefit from surgery, but a progressive improvement in both axial and limb dystonia began within 3 days. The Burke-Fahn-Marsden scores were 75 (maximum possible = 120) at baseline, 52 at 5 days, and 16 at 3 months after surgery. The mechanism of action of pallidotomy for dystonia and the reasons for the delayed and progressive improvement are unknown. Nevertheless, the magnitude of the improvement and the safety of the procedure in this one patient warrant a careful evaluation of pallidotomy for dystonia.

Anesthesia, General↗
PubMed1997

The role of botulinum toxin in the treatment of lower limb spasticity in children with cerebral palsy--a pilot study.

The use of botulinum toxin in cerebral palsy is still experimental. We conducted a pilot clinical trial with botulinum toxin injections on 14 children with spastic cerebral palsy. All patients were mobile with dynamic contractures of the gastrocnemius-soleus muscles. The injections were monophasic in 9 patients and biphasic in 5 patients. Improvement in dorsiflexion, quality of gait and grade of independence were achieved in 3 patients; improvement in dorsilflexion and quality of gait were achieved in 6 patients. There was no significant change in quality of gait in 4 patients. The beneficial effect lasted 4-9 months (mean 6.7 months). A combined functional score given by the physicians, therapists and parents showed a marked improvement in 6 patients (42.9%), a mild improvement in 3 patients (21.4%) and no improvement in 5 patients (35.7%). Biphasic injections were slightly more effective than monophasic injections (p < 0.02). Adverse effects were usually mild. We conclude that botulinum toxin may be used for the reduction of spasticity in patients with cerebral palsy who have dynamic deformities of the ankle joints.

Activities of Daily Living↗
PubMed1996

Occurrence of Parkinson's syndrome in type I Gaucher disease.

Gaucher disease, the most prevalent glycolipid storage disorder, is classically subdivided into types according to the presence or absence of neurological involvement. Type I has hitherto been considered non-neuronopathic. We present six cases and a review of the literature of Parkinsonian symptoms in type I Gaucher disease patients. The hallmark of this atypical Parkinsonian syndrome is a relatively severe clinical course with early appearance of neurological signs in the 4th to 6th decade of life, aggressive progression of the signs and refractoriness to conventional anti-Parkinson therapy. We discuss the implications of these findings in the light of enzyme replacement therapy for Gaucher disease.

Adolescent↗
PubMed1994

Metabolic topography of the hemiparkinsonism-hemiatrophy syndrome.

We estimated regional and global metabolic rates for glucose using 18F-fluorodeoxyglucose (FDG) and PET in six patients with hemiparkinsonism-hemiatrophy syndrome (HPHA; mean age, 41.0 +/- 12.4 years). We used 18F-fluorodopa (FDOPA) and PET in two patients to quantify presynaptic nigrostriatal dopaminergic function. We compared measures of brain glucose metabolism and striatal FDOPA uptake with those calculated for 10 age-matched normal volunteers (mean age, 35.1 +/- 8.0 years) and 10 patients with typical unilateral Parkinson's disease (unilat-PD; mean age, 58.2 +/- 13.8 years). All six HPHA patients demonstrated significant metabolic reductions (> 3 SD) in the contralateral basal ganglia or frontal cortex as compared with normal control values. Mean normalized glucose metabolism was reduced in the contralateral caudate and lentiform nuclei (p < 0.005) as compared with that in unilat-PD and normal controls. In both patients studied with FDOPA, contralateral striatal uptake was significantly reduced (> 3 SD) as compared with normal control values. These results suggest that the clinical manifestations of HPHA arise through a combination of pre- and postsynaptic nigrostriatal dopaminergic dysfunction. FDG and PET may be useful in differentiating this disorder from typical unilat-PD.

Adult↗
PubMed1994

Interventional neurology: botulinum toxin as a potent symptomatic treatment in neurology.

Local injections of botulinum toxin is a well-accepted treatment for focal dystonias, hemifacial spasms and strabismus. Its use by skilled neurologists has been reported to be safe and effective. We report our experience with botulinum toxin injections in 108 patients with various central nervous system disorders. Botox was effective in upper face dystonia (86% improvement), spastic dysphonia (92% improvement), platysma muscle spasms and spasmodic torticollis (range of movement 61%, pain and tension 90%). It was also very effective in a few patients with apraxia of eyelid opening, parkinsonian jaw tremor, teeth clenching, palatal myoclonus and adductor leg spasticity. No serious side effects were recorded. Botulinum toxin is a useful symptomatic treatment for many neurological disorders, and one of the leading mode of treatments in the new subspecialty in neurology called "Interventional neurology."

Adolescent↗
PubMed1993

[Botulinum toxin for palatal myoclonus and spastic dysphonia].

Botulinum toxin (B; Botox), produced by the anaerobic bacterium Clostridium botulinum, causes temporary paralysis by blocking the presynaptic release of acetylcholine at the neuromuscular junction. This action is clinically used to alleviate muscle spasm by injecting the toxin directly into the overactive muscle. We report our experience with B injections in 2 women, aged 20 and 21, respectively, 1 of whom had bilateral palatal myoclonus and the other adductor spastic dysphonia. Both showed remarkable improvement of conditions for which, until now, we had no effective treatment. These are the first cases in Israel treated with B for otorhinolaryngological conditions.

Adult↗
PubMed1993

Brain glucose metabolism and dopamine D2 receptor analysis in a patient with hemiparkinsonism-hemiatrophy syndrome.

We report findings on brain glucose metabolism and dopamine D2 receptors generated by positron emission tomography (PET) in a 67-year-old woman with right hemiparkinsonism-hemiatrophy syndrome (HP-HA). PET with [18F]-fluorodeoxyglucose (FDG) showed marked glucose metabolism asymmetry. There were significant reductions in glucose uptake at the level of the basal ganglia and, to lesser extent, in the fronto-parietal cortex contralateral to the clinically involved side. These changes were different from those found in a patient with hemi-Parkinson's disease who was scanned under similar conditions. Because the patient with HP-HA had only minimal response to levodopa therapy, we evaluated post-synaptic dopaminergic structures using PET with [18F]-fluoroethylspiperone (FESP). No striatal binding asymmetry was found in FESP/PET, which suggests a sparing of striatal dopamine D2 receptors. The changes in FDG uptake which we found were in brain areas relevant to the clinical features of HP-HA syndrome. In addition, our study provides evidence that FDG/PET may help to differentiate HP-HA syndrome from hemi-Parkinson's disease. In most instances, since HP-HA is associated with a more benign clinical course than Parkinson's disease, this distinction is of clinical important.

Aged↗
PubMed1992

Motor blocks in Parkinson's disease.

Freezing episodes and related phenomena (as a general term, motor blocks [MBs]) are poorly understood, particularly disabling, and a therapeutically frustrating problem in Parkinson's disease (PD). Epidemiologic and clinical characteristics of MBs, as well as risk factors to develop MBs, have never been fully addressed. Herein, we report our database survey on 990 PD patients, of whom 318 (32%) had MBs. The majority of MBs were linked to gait. Start hesitation occurred in 86%, blocking on turning in 45%, and blocking in narrow spaces in 25% of patients. Initial parkinsonian symptoms in the upper body and tremor as the initial motor symptom were less likely to be associated with the presence of MBs (odds ratios [OR] 0.6 and 0.7, respectively), while initial symptoms affecting gait or trunk had higher association with MBs (OR = 1.58). Longer disease duration, higher Hoehn and Yahr stage, and longer duration of levodopa treatment are all significantly associated with the presence of MBs. We observed significant association between the existence of MBs and levodopa-induced dyskinesias to suggest similar pathophysiology. We propose that MBs in PD are abnormal retrieval or execution of complex motor tasks that can occur as a result of disease progression or as short- or long-term side effects of levodopa treatment.

Dyskinesia, Drug-Induced↗
PubMed1991

Myelopathy as a complication of diabetes mellitus.

Clinical signs of spinal cord involvement in diabetes mellitus have gained very little attention in the past four decades. On the other hand many pathological studies have shown spinal cord lesions in diabetic patients. We report 12 diabetic patients with clinical signs of myelopathy which, per exclusion, could be explained only as related to diabetes mellitus. Posterior column lesions were more common than corticospinal tract involvement. All our patients had combined peripheral sensory polyneuropathy with myelopathic signs. The combination of peripheral neuropathy, disturbed sense of position and/or vibration with pyramidal signs is highly suggestive of diabetic myelopathy with polyneuropathy. Even though myelopathy is not common in diabetic patients, it is one of the most debilitating neurological complications of diabetes mellitus. We believe that there is enough pathological and clinical evidence to accept the concept of diabetic myelopathy, especially with its prognostic and rehabilitative implications.

Adult↗