Search PubMed⌕ Search

Biomedical subjects

N Giladi

Publications and source records attributed to N Giladi.

At least 55 records · Page 3Linked to original sources
PubMed2000

Construction of freezing of gait questionnaire for patients with Parkinsonism.

Background: Freezing of gait (FOG) is a common, poorly understood, parkinsonian symptom interfering with daily functioning and quality of life. Assessment of FOG is complex because of the episodic nature of this symptom, and the influence of mental and environmental factors on it.Objective: To design a self-reportable reliable questionnaire for FOG.Method: A questionnaire consisting of 16 items regarding gait and falls was administered together with the Unified Parkinson's Disease Rating Scale (UPDRS) to 40 Parkinson's disease (PD) patients (26 males) with a mean age of 72.3+/-9.3 years and mean Hoehn and Yahr (H&Y) stage at "Off" of 2.85+/-0.84. A principal component analysis with Varimax rotation was conducted on the results. Item analyses were performed and reliability computed for an abbreviated FOG questionnaire.Results: Based on these analyses, a short (six item) FOG questionnaire was constructed, which was found to be highly reliable (Cronbach alpha=0.94) for assessment of FOG and with moderate correlation with the activity of daily living (ADL) and motor parts of the UPDRS (0.43 and 0.40, respectively). Moderate correlation was also found with the FOG item at the ADL part of the UPDRS (alpha=0.66 for the "Off" and 0.77 for the "On" state).Conclusion: The FOG questionnaire that was constructed is highly reliable in assessing freezing of gait, unrelated to falls, in patients with PD.

Journal Article↗
PubMed2000

[Botulin toxin for spasticity in spinal cord damage by treating the motor endplate].

Therapeutic injection of botulin toxin is well-recognized for reducing tonus in local dystonia. However, its efficacy in reducing spasticity in spinal cord injuries is still unproven. 4 men and 1 woman (mean age 39 years, range 20-56) with spinal cord injury and debilitating spasticity, and no response to standard treatment for spasticity received injections of botulin, 200-300 U, into 4-8 points in their legs to block muscle-nerve synapses. In all 5 tonus was reduced in the area of the block, while in some it was also reduced in more distal muscles. In 1 there was reduced tonus in both the injected and contralateral leg. The therapeutic effect on tonus persisted for 3 months. In spite of objective improvement in tonus in all 5, only 3 felt subjective improvement, but in none was there improvement on standard functional scaling. We found injection of botulin toxin effective in reducing tonus in the spinal cord-injured, and to some extent in improving subjective feeling of well-being in some of them. Objective measurement might show functional improvement after larger doses of toxin injected into more muscles. This might be necessary because the muscle mass of the legs is large and the intensity of involuntary contraction is especially high in these patients.

Adult↗
PubMed2000

Anal sphincter EMG does not distinguish between multiple system atrophy and Parkinson's disease.

Clinical distinction of multiple system atrophy (MSA) from Parkinson's disease (PD) is often difficult. Several recent reports indicate that objective classification may be accomplished using electromyographic (EMG) testing of the anal or urethral sphincters, but some authors have found that these tests are not reliable for this purpose. We studied 13 patients with PD and 10 with probable MSA, as diagnosed by consensus of four movement disorders specialists, according to accepted clinical criteria. Anal sphincter EMG was performed blind to the clinical diagnosis. We found no significant differences in the mean duration of motor unit potentials (MUPs), mean MUP amplitude, or prevalence of polyphasic potentials, satellite potentials, very long duration MUPs, or spontaneous activity between the two groups. Thus, anal sphincter EMG does not differentiate between PD and MSA.

Aged↗
PubMed2000

Risk factors for dementia, depression and psychosis in long-standing Parkinson's disease.

OBJECTIVES: To study the relationships between clinical features of Parkinson's disease (PD) and the development of dementia, depression or psychosis in patients with long-standing disease. BACKGROUND: The natural history of dementia and depression in PD, and its relation to psychosis in long standing PD, are unclear. METHOD: 172 consecutive patients (99 men and 73 women, mean age at symptoms onset 58.3 +/- 13.2 years) with 5 years or more of PD (mean symptom duration of 11.8 +/- 5.6 years) were studied. Clinical data were collected during the last office visit through physical examination, detailed history, review of patient charts and outside documents. Dementia and depression were diagnosed according to DSM-IV criteria, while psychosis was diagnosed if hallucinations or delusions were present. Chi-square and t tests were used to compare the patient characteristics among those with vs. those without mental complications of the disease at different disease stages. Logistic regression was used for the comparison of associations between the presence of dementia or depression (dependent variable) and age at onset of PD, duration of PD and disease staging (explanatory variables). RESULTS: The study population consisted of 45 patients at Hoehn & Yahr (H&Y) stage < or = 2.5 (26%), 104 patients at stage 3 (60.5%) and 23 patients at H&Y stage 4-5 (13.5%). Sixty one patients (36%) had dementia, 55 patients had depression (33%) and 50 patients (27%) had psychosis. Dementia and depression were significantly associated with disease severity as reflected in the H&Y scale (P = 0.0003, Z = 3.59; P = 0.006, Z = 3.22, respectively). These associations were significant also for the older age of PD onset (> or = 59 years n = 89) subgroup (p = 0.001, Z = 3.2 for dementia and p = 0.02, Z = 2.9 for depression), but not for younger onset cases (< 59 years n = 83). Dementia was significantly associated with older age of PD onset (beta = 0.04, p = 0.009) while depression was inversely associated with age of PD onset (beta = -0.04, p = 0.02). The presence of dementia was also significantly associated with depression (beta = 1.49, p = 0.0006). Dementia and depression were found to be independent explanatory variables for the development of psychosis (logistic regression, odds ratio (OR) = 26.0, p < 0.0001; OR = 10.2, p < 0.0001, respectively). In patients with younger age of PD onset, depression more than dementia was strongly correlated with the appearance of psychosis. CONCLUSION: Dementia in PD was related to older age of symptoms onset and old age. Depression was associated with dementia or early age of PD onset. Depression seemed to contribute to the appearance of psychosis even more than dementia, especially in patients with younger age of symptoms onset.

Age Distribution↗
PubMed2000

Long-term remission of idiopathic cervical dystonia after treatment with botulinum toxin.

Botulinum toxin type A (BTX-A) treatment for cervical dystonia is traditionally considered a purely symptomatic treatment. BTX-A blocks acetyl choline exocytosis for 3-6 months and most patients require reinjection after this period. We report on 6 patients (mean age 41.6 years, range 18-69) with idiopathic cervical dystonia who were treated with BTX-A injections and became asymptomatic for 2-4 years. Four patients showed remission after the first BTX-A treatment, 1 patient after the second set of injections and 1 after the third session. Amelioration of neck dystonia was observed within 1-4 weeks after the last BTX-A treatment and all 6 patients are symptom-free, off antidystonic medications for over 2 years. The possibility that BTX-A treatment may increase the chances of development of clinical remission in patients with idiopathic cervical dystonia is discussed.

Adolescent↗
PubMed2000

Use of the selective serotonin 3 receptor antagonist ondansetron in the treatment of neuroleptic-induced tardive dyskinesia.

OBJECTIVE: The authors examined the efficacy, tolerability, and safety of ondansetron, a selective serotonin 3 receptor antagonist, in patients with tardive dyskinesia. METHOD: Twenty patients with schizophrenia who had neuroleptic-induced tardive dyskinesia were given 12 mg/day of ondansetron for 12 weeks in an open-label study. RESULTS: Administration of ondansetron resulted in a statistically significant improvement in tardive dyskinesia and psychotic symptoms. CONCLUSIONS: Ondansetron may be an effective and safe therapy to control tardive dyskinesia and psychosis in patients with schizophrenia.

Adult↗
PubMed2000

Young women with PD: a group work experience.

Parkinson's Disease (PD) prior to the age of 40 affects between 5-10% of the PD population. The psychosocial changes that patients with early PD encounter, may be more devastating and disabling than the actual motor disability. The paper describes a unique experience in groupwork with young female PD patients treated in the Movement Disorders Unit of the Tel Aviv Sourasky Medical Center. The paper focuses on the special issues which characterized this group's experience: stigma, body and sexual image, and personality traits.

Adaptation, Psychological↗
PubMed2000

Hereditary juvenile-onset craniocervical predominant generalized dystonia with parkinsonism.

OBJECTIVE: To report a unique hereditary, juvenile onset, craniocervical predominant, generalized dystonia and parkinsonism affecting four members of one family. FAMILY DESCRIPTION: A father and three of his four daughters presented to us over the past 30 years with a similar picture of generalized dystonia, starting in the craniocervical region in the second or third decade of life. They later developed moderate parkinsonism, mainly manifesting bradykinesia, rigidity and abnormal postural reflexes. Biochemical and genetic tests excluded Wilson's disease, Huntington's disease and Oppenheim's dystonia. CONCLUSION: This is a new type of familial dystonia-parkinsonism where the craniocervical dystonic symptoms are most prominent in the early stages while parkinsonism becomes the predominant problem later in life. A search for the genetic mutation in this family is underway.

Adolescent↗
PubMed1999

Absence of mutations in ATM, the gene responsible for ataxia telangiectasia in patients with cerebellar ataxia.

Ataxia-telangiectasia (AT) is an autosomal recessive multisystem disorder presenting in childhood with progressive cerebellar ataxia, oculocutaneous telangiectasia, immune deficiency, radiosensitivity, and cancer predisposition. The gene for AT, designated ATM (AT, mutated) encodes a protein with a carboxy-terminal phosphoinositide-3 kinase domain which is involved in cell cycle checkpoints and other responses to genotoxic stress. Most of the patients with the classical AT phenotype are homozygous or compound heterozygous for severe mutations causing truncation or destabilization of the ATM protein. Patients with a milder forms of disease, called AT variants, have been found to be either homozygous for milder mutations or compound heterozygotes for null alleles and mild mutations. In order to define the clinical phenotype of patients homozygous (or compound heterozygotes) for other, milder mutations, we decided to search for ATM mutations in patients with either sporadic or familial idiopathic ataxia. Thirty-four patients with idiopathic cerebellar ataxia, aged 3-77 years, were screened for mutations in the ATM coding region. There were 12 familial cases. None of the patients had abnormal immunoglobulin or alpha-fetoprotein levels, and none had mutations in the ATM coding region. In this heterogeneous group of patients with cerebellar ataxia we found no mutations in the ATM gene. We conclude that mutations in the ATM gene are probably not a common cause for cerebellar ataxia other than AT.

Adolescent↗
PubMed1998

Deprenyl monotherapy improves visuo-motor control in early parkinsonism.

Deprenyl is a potent MAO-B inhibitor which is commonly prescribed for treatment of parkinsonism. Despite prevalent use its effects on the symptoms and course of Parkinson's disease (PD) are still debated. The present study was therefore undertaken in order to measure quantitatively changes in visuo-motor control (VMC), consequent to deprenyl monotherapy in early PD. Previous work from our laboratory has shown typical VMC deterioration in PD patients, that correlates with disease severity. Thus, measurements of such changes provides a sensitive tool with which the symptomatic effects of drug treatment can be assessed quantitatively. Fourteen newly diagnosed, PD patients with light symptoms were studied. The VMC of all patients was tested after the first neurological examination, before drug treatment commenced. A second test was done after 30 days of treatment with deprenyl at a dose of 2.5 mg/day. Following this test, dosage was increased to 10 mg/day and a third VMC test was given after 30 more days of treatment. Our results show significant improvement in VMC functions following 30 days of 2.5 mg/day treatment and a continuing improvement after the next 30 days of 10 mg/day treatment. This improvement pertains mainly to directional control of self initiated movements and is smaller for movements that are guided externally. We conclude that deprenyl monotherapy has a clear symptomatic beneficial effect for patients with early PD.

Antiparkinson Agents↗
PubMed1998

Visuomotor control abnormalities in patients with unilateral parkinsonism.

Visuomotor performance is known to be disturbed in patients who have advanced Parkinson's disease (PD). The degree of impairment in the early stages of PD was investigated in both the symptomatic and asymptomatic hand of patients with unilateral disease. We examined the visuomotor performance of 10 early unilateral parkinsonian patients and 15 control subjects by using several tracing and tracking tasks that were performed with unseen hands, in which feedback was given through a screen cursor. Significant impairment in control of movement direction was found in tracing of screen paths but not in tracking. Significant slowing of movement was found in target tracking, whereas tracing velocity was normal. Although all patients were judged by standard clinical criteria to be unilaterally affected, visuomotor functions were found to be impaired equally in both hands. Visuomotor control of movement direction and movement velocity is performed independently. Performance along both control dimensions is impaired in the mild stages of parkinsonism, even before the appearance of motor symptoms.

Aged↗
PubMed1998

[Botulinum toxin injection effective for post-peripheral facial nerve palsy synkinesis].

Facial synkinesis is an involuntary activation of muscles innervated by the zygomatic or mandibular branch of the facial nerve in conjunction with voluntary activation of the other branch. It appears frequently after recovery from peripheral facial nerve paralysis. We report 10 patients with facial synkinesis following Bell's palsy with a mean duration of synkinesis of 7 +/- 4 years before treatment with periorbital injections of Botulinum toxin type A. 9 had marked subjective and objective improvement starting a few days after injection and lasting 4-9 months. The results suggest a useful treatment option for post-Bell's palsy facial synkinesis with Botulinum toxin type A.

Botulinum Toxins↗
PubMed1997

The mechanism of action of botulinum toxin type A in focal dystonia is most probably through its dual effect on efferent (motor) and afferent pathways at the injected site.

OBJECTIVE: To highlight some clinical and physiological features related to treatment with botulinum toxin type A (BTX-A) injections for focal dystonia that may suggest an effect through efferent (alpha motoneuron) and afferent pathways. DATA SOURCES: This review is based on published clinical and physiological studies as well as personal experience regarding the effect of BTX-A in focal dystonia. DATA SYNTHESIS: Long or short lag period between BTX-A injections and clinical improvement, remote effect, an effect on the basic physiological characteristics of dystonia, poor correlation between the local weakness and the clinical improvement and alleviation of pain are clinical observations which are difficult to explain on the basis of the known effect of BTX-A on the neuromuscular junction of the alpha motoneuron. These observations as well as recent scientific reports are used to discuss a hypothesis that in addition to its effect as local muscle relaxant, BTX-A acts at the level of the central nervous system (CNS) for 'reorganization'. Such an effect on CNS activity can be mediated through afferent pathways coming from the injected site--possibly originated in muscle spindles. Its effect through afferent pathways on the CNS may be considered as a long-term 'sensory trick'.

Afferent Pathways↗