*  The Influence of Deep TMS on Cerebellar Signs in Patients With Machado Joseph Disease - Full Text View - ClinicalTrials.gov

Cerebellar Ataxia. Cerebellar Diseases. Brain Diseases. Central Nervous System Diseases. Nervous System Diseases. ... The Influence of Deep TMS on Cerebellar Signs in Patients With Machado Joseph Disease. The recruitment status of this study is ... Spinal Cord Diseases. Heredodegenerative Disorders, Nervous System. Neurodegenerative Diseases. Ataxia. Dyskinesias. Neurologic ... Genetics Home Reference related topics: VLDLR-associated cerebellar hypoplasia autosomal recessive cerebellar ataxia type 1 ...
https://clinicaltrials.gov/ct2/show/NCT02039206?recr=Open&cond="Cerebellar Diseases"&rank=3

*  DMOZ - Health: Conditions and Diseases: Neurological Disorders: Brain Diseases: Cerebellar

Cardinal manifestations of cerebellar dysfunction include dysmetria, gait ataxia, and muscle hypotonia. ... Diseases that affect the structure or function of the cerebellum. ... Diseases that affect the structure or function of the cerebellum. Cardinal manifestations of cerebellar dysfunction include ... NIH: Ataxias and Cerebellar/Spinocerebellar Degeneration Information sheet compiled by the National Institute of Neurological ...

*  DMOZ - Health: Animal: Mammals: Cats: Conditions and Diseases: Cerebellar Hypoplasia

"Health ... Cerebellar Hypoplasia" search on: AOL - Ask - Bing - DuckDuckGo - Gigablast - Google - ixquick - Yahoo - Yandex - ...

*  DMOZ - Health: Conditions and Diseases: Cancer: Brain and CNS: Brain Tumor, Childhood: Cerebellar Astrocytoma

Health Conditions and Diseases Cancer Brain and CNS Brain Tumor, Childhood Cerebellar Astrocytoma 1 ... "Health ... Cerebellar Astrocytoma" search on: AOL - Ask - Bing - DuckDuckGo - Gigablast - Google - ixquick - Yahoo - Yandex - ...

*  Safety and Efficacy of Umbilical Cord Mesenchymal Stem Cell Therapy for Patients With Hereditary Ataxia - Full Text View -...

Nervous System Diseases. Signs and Symptoms. Cerebellar Diseases. Brain Diseases. Central Nervous System Diseases. Spinal Cord ... Genetics Home Reference related topics: VLDLR-associated cerebellar hypoplasia autosomal recessive cerebellar ataxia type 1 ... Cerebellar Ataxia. Spinocerebellar Degenerations. Dyskinesias. Neurologic Manifestations. ...

*  Efficacy of Riluzole in Hereditary Cerebellar Ataxia - Full Text View - ClinicalTrials.gov

Nervous System Diseases. Signs and Symptoms. Brain Diseases. Central Nervous System Diseases. Spinal Cord Diseases. ... Cerebellar Ataxia. Spinocerebellar Degenerations. Cerebellar Diseases. Ataxia. Dyskinesias. Neurologic Manifestations. ... Purkinje cells project inhibitory signals to the deep cerebellar nuclei(DCN) which have a critical role in cerebellar function ... Neurodegenerative Diseases. Genetic Diseases, Inborn. Riluzole. Anticonvulsants. Excitatory Amino Acid Antagonists. Excitatory ...
https://clinicaltrials.gov/ct2/show/NCT01104649?term=Cerebellar Degeneration&rank=15

*  A 24-week Open-label Study of KPS-0373 in Patients With Spinocerebellar Degeneration (SCD) - Full Text View - ClinicalTrials.gov

Cerebellar Diseases. Brain Diseases. Central Nervous System Diseases. Nervous System Diseases. Spinal Cord Diseases. ... Neurodegenerative Diseases. Genetic Diseases, Inborn. Cerebellar Ataxia. Ataxia. Dyskinesias. Neurologic Manifestations. ... Genetics Home Reference related topics: VLDLR-associated cerebellar hypoplasia autosomal recessive cerebellar ataxia type 1 ...
https://clinicaltrials.gov/ct2/show/NCT01970137?cond="infantile-onset spinocerebellar ataxia" OR "Spinocerebellar Ataxias"&rank=18

*  International Ataxia Rating Scale in Younger Patients - Full Text View - ClinicalTrials.gov

Cerebellar Diseases. Brain Diseases. Central Nervous System Diseases. Vascular Diseases. Cardiovascular Diseases. ... Cerebellar Ataxia. Telangiectasis. Ataxia Telangiectasia. Dyskinesias. Neurologic Manifestations. Nervous System Diseases. ... Genetic Diseases, Inborn. DNA Repair-Deficiency Disorders. Metabolic Diseases. Immunologic Deficiency Syndromes. Immune System ... Children aged 6-18 years with AT like disease, with or without proven mutation in the MRE11 gene will be included ...
https://clinicaltrials.gov/ct2/show/NCT01942850?recr=Open&cond="Cerebellar Diseases"&rank=14

*  Efficacy Study of Epoetin Alfa in Friedreich Ataxia - Full Text View - ClinicalTrials.gov

Nervous System Diseases. Signs and Symptoms. Cerebellar Diseases. Brain Diseases. Central Nervous System Diseases. ... Neurodegenerative Diseases. Genetic Diseases, Inborn. Mitochondrial Diseases. Metabolic Diseases. Epoetin Alfa. Hematinics. ... Genetics Home Reference related topics: Friedreich ataxia VLDLR-associated cerebellar hypoplasia autosomal recessive cerebellar ... Any acute/chronic disease that might interfere with the clinical trial, as judged by the investigator ...

*  James D. Bowen, MD | Swedish Medical Center Seattle and Issaquah

... and these descriptions of the disease course no longer meet our needs to describe the disease.. Over the past couple of years, ... and were not based on any particular understanding of the biology of the disease, the cause of the disease, or even the ... Jim Bowen has always been very involved with my health, as it pertains to my disease. He is professional, up to date on all ... On March 27, the U.S. Food and Drug Administration approved the newest treatment in the increasing number of disease modifying ...
swedish.org/swedish-physicians/profile.aspx?name=bowen james d&id=160896

*  Medicowesome: The basics :Parkinson's disease

Characteristics features is tremors .Tremors occurs during all walking hours and therefore it is a type of involuntary tremor in case of cerebellar disease there is an intension tremor because tremors are seen when patient perform any work ...

*  Data from: Inferior cerebellar hypoplasia resembling a Dandy-Walker-like malformation in purebred Eurasier dogs with familial...

Cerebellar malformations can be inherited or caused by insults during cerebellar development. To date, only sporadic cases of cerebellar malformations have been reported in dogs, and the genetic background has remained obscure. Therefore, this study`s objective was to describe the clinical characteristics, imaging features and pedigree data of a familial cerebellar hypoplasia in purebred Eurasier dogs. A uniform cerebellar malformation characterized by consistent absence of the caudal portions of the cerebellar vermis and, to a lesser degree, the caudal portions of the cerebellar hemispheres in association with large retrocerebellar fluid accumulations was recognized in 14 closely related Eurasier dogs. Hydrocephalus was an additional feature in some dogs. All dogs displayed non-progressive ataxia, which had already been noted when the dogs were 5 - 6 weeks old. The severity ...

(1/486) Non-motor associative learning in patients with isolated degenerative cerebellar disease.

In recent decades it has become clear that the cerebellum is involved in associative motor learning, but its exact role in motor learning as such is still controversial. Recently, a contribution of the cerebellum to different cognitive abilities has also been considered, but it remains unclear whether the cerebellum contributes to cognitive associative learning. We compared nine patients with an isolated cerebellar degenerative disease in a cognitive associative learning task with 10 controls. Patients and controls were matched for age, sex, handedness, level of education, intelligence and capabilities of visual memory. The subjects were asked to learn the association between six pairs of colours and numerals by trial and error. Additionally, a simple reaction time and a visual scanning test were conducted in order to control for the influence of motor performance deficits in cerebellar patients. In comparison with the controls, it took the patients significantly longer to learn the correct associations between colours and numerals, and they were impaired in recognizing them later on. Two patients showed no associative learning effect at all. Neither the simple reaction time nor the visual scanning time correlated substantially with the results of associative learning. Therefore, motor-associated disabilities are unlikely to be the reason for the learning deficit in cerebellar patients. Our results suggest that the cerebellum might contribute to motor-independent processes that are generally involved in associative learning.  (+info)

(2/486) Contralateral deafness following unilateral suboccipital brain tumor surgery in a patient with large vestibular aqueduct--case report.

A 68-year-old female developed contralateral deafness following extirpation of a left cerebellopontine angle epidermoid cyst. Computed tomography showed that large vestibular aqueduct was present. This unusual complication may have been caused by an abrupt pressure change after cerebrospinal fluid release, which was transmitted through the large vestibular aqueduct and resulted in cochlear damage.  (+info)

(3/486) Anticonvulsant-induced dyskinesias: a comparison with dyskinesias induced by neuroleptics.

Anticonvulsants cause dyskinesias more commonly than has been appreciated. Diphenylhydantoin (DPH), carbamazepine, primidone, and phenobarbitone may cause asterixis. DPH, but not other anticonvulsants, may cause orofacial dyskinesias, limb chorea, and dystonia in intoxicated patients. These dyskinesias are similar to those caused by neuroleptic drugs and may be related to dopamine antagonistic properties possessed by DPH.  (+info)

(4/486) Intrameatal aneurysm successfully treated by meatal loop trapping--case report.

A 77-year-old female presented with a rare intrameatal aneurysm manifesting as sudden onset of headache, hearing loss, tinnitus, and vertigo associated with subarachnoid hemorrhage. Meatal loop trapping was performed. After surgery, the patient's functions recovered almost completely, probably because of the preservation of the 7th and 8th cranial nerves and the presence of effective collaterals in the area supplied by the anterior inferior cerebellar artery.  (+info)

(5/486) Remote regional cerebral blood flow consequences of focused infarcts of the medulla, pons and cerebellum.

The aim of this study was to evaluate regional and remote diaschisis of inferior brain stem or cerebellar infarcts in 25 patients presenting with relatively limited lesions. Patients presented with medullary, pontine or cerebellar infarction. METHODS: Lesions were evaluated on MRI (0.5 T). Regional cerebral blood flow (rCBF) was assessed by means of SPECT, after injection of 9rmTc-hexamethyl propyleneamine oxime (HMPAO) and, when possible, inhalation of 133Xe in the same session. For each method, asymmetry indices (Als), comparing contralateral to ipsilateral rCBF values, were calculated in four areas of each cerebral hemisphere and in the cerebellum and later compared with values obtained in healthy subjects (P = 0.05). RESULTS: Higher rCBF values were observed in the contralateral cerebellum in 2 of 7 patients with selective lateral medullary lesions, and cerebellar Als were significantly increased. When a cerebellar infarct was associated with a lateral medullary lesion, the cerebellar and contralateral hemispheric asymmetries were more severe. Unilateral paramedian pontine infarcts had more frequent consequences on the cerebellum (2 of 3 cases), with rCBF or tracer uptake being reduced in the ipsilateral or the contralateral lobe. Inverse cerebral hemispheric asymmetry could then be observed. Bilateral pontine lesions were difficult to evaluate. Using 99mTc-HMPAO, discrete cerebellar asymmetry was observed in 3 of 6 cases. Pure cerebellar infarcts in the posterior inferior cerebellar artery territory were always associated with a severe ipsilateral flow drop in the cerebellum, and contralateral hemispheric diaschisis was frequent (3 of 4 patients), predominating in the frontotemporal cortex and subcortical structures. This was also more obvious using 99mTC-HMPAO than 133Xe. Variance analysis showed that hemispheric diaschisis was more severe in mixed brain stem and cerebellar infarcts than in pure cerebellar or brain stem lesions. Furthermore, cerebellar and hemispheric AI values were not correlated with measurements of clinical deficits, disability or handicap. CONCLUSION: Unilateral and limited inferior brain stem lesions can have ipsi- or contralateral consequences on the cerebellum and cerebral hemispheres rCBF. These remote effects are related to lesions of the main pathways joining these structures, resulting in deactivation and, in some cases, overactivation. Contrary to what has been suggested, consequences on cerebral hemispheres are more severe in mixed cerebellar and brain stem infarcts than in pure cerebellar lesions.  (+info)

(6/486) Multiple large and small cerebellar infarcts.

To assess the clinical, topographical, and aetiological features of multiple cerebellar infarcts,18 patients (16.5% of patients with cerebellar infarction) were collected from a prospective acute stroke registry, using a standard investigation protocol including MRI and magnetic resonance angiography. Infarcts in the posterior inferior cerebellar artery (PICA)+superior cerebellar artery (SCA) territory were most common (9/18; 50%), followed by PICA+anterior inferior cerebellar artery (AICA)+SCA territory infarcts (6/18; 33%). One patient had bilateral AICA infarcts. No infarct involved the PICA+AICA combined territory. Other infarcts in the posterior circulation were present in half of the patients and the clinical presentation largely depended on them. Large artery disease was the main aetiology. Our findings emphasised the common occurrence of very small multiple cerebellar infarcts (<2 cm diameter). These very small multiple cerebellar infarcts may occur with (13 patients/18; 72%) or without (3/18; 22%) territorial cerebellar infarcts. Unlike previous series, they could not all be considered junctional infarcts (between two main cerebellar artery territories: 51/91), but also small territorial infarcts (40/91). It is suggested that these very small territorial infarcts may be endzone infarcts, due to the involvement of small distal arterial branches. It is possible that some very small territorial infarcts may be due to a microembolic process, but this hypothesis needs pathological confirmation.  (+info)

(7/486) Failure of cerebellar patients to time finger opening precisely causes ball high-low inaccuracy in overarm throws.

We investigated the idea that the cerebellum is required for precise timing of fast skilled arm movements by studying one situation where timing precision is required, namely finger opening in overarm throwing. Specifically, we tested the hypothesis that in overarm throws made by cerebellar patients, ball high-low inaccuracy is due to disordered timing of finger opening. Six cerebellar patients and six matched control subjects were instructed to throw tennis balls at three different speeds from a seated position while angular positions in three dimensions of five arm segments were recorded at 1,000 Hz with the search-coil technique. Cerebellar patients threw more slowly than controls, were markedly less accurate, had more variable hand trajectories, and showed increased variability in the timing, amplitude, and velocity of finger opening. Ball high-low inaccuracy was not related to variability in the height or direction of the hand trajectory or to variability in finger amplitude or velocity. Instead, the cause was variable timing of finger opening and thereby ball release occurring on a flattened arc hand trajectory. The ranges of finger opening times and ball release times (timing windows) for 95% of the throws were on average four to five times longer for cerebellar patients; e.g., across subjects mean ball release timing windows for throws made under the medium-speed instruction were 11 ms for controls and 55 ms for cerebellar patients. This increased timing variability could not be explained by disorder in control of force at the fingers. Because finger opening in throwing is likely controlled by a central command, the results implicate the cerebellum in timing the central command that initiates finger opening in this fast skilled multijoint arm movement.  (+info)

(8/486) Preserved performance by cerebellar patients on tests of word generation, discrimination learning, and attention.

Recent theories suggest that the human cerebellum may contribute to the performance of cognitive tasks. We tested a group of adult patients with cerebellar damage attributable to stroke, tumor, or atrophy on four experiments involving verbal learning or attention shifting. In experiment 1, a verb generation task, participants produced semantically related verbs when presented with a list of nouns. With successive blocks of practice responding to the same set of stimuli, both groups, including a subset of cerebellar patients with unilateral right hemisphere lesions, improved their response times. In experiment 2, a verbal discrimination task, participants learned by trial and error to pick the target words from a set of word pairs. When age was taken into account, there were no performance differences between cerebellar patients and control subjects. In experiment 3, measures of spatial attention shifting were obtained under both exogenous and endogenous cueing conditions. Cerebellar patients and control subjects showed similar costs and benefits in both cueing conditions and at all SOAs. In experiment 4, intra- and interdimensional shifts of nonspatial attention were elicited by presenting word cues before the appearance of a target. Performance was substantially similar for cerebellar patients and control subjects. These results are presented as a cautionary note. The experiments failed to provide support for current hypotheses regarding the role of the cerebellum in verbal learning or attention. Alternative interpretations of previous results are discussed.  (+info)


  • Cardinal manifestations of cerebellar dysfunction include dysmetria, gait ataxia, and muscle hypotonia. (dmoztools.net)
  • DCN neurons fire spontaneously in the absence of synaptic input from Purkinje neurons and modulation of the DCN response by Purkinje input is believed to be responsible for coordination of movement, while uncontrolled spontaneous firing of DCN neurons may underlay cerebellar ataxia. (clinicaltrials.gov)
  • Since SK channels are critical regulators of DCN firing rate, SK openers such as the drug riluzole may reduce neuronal hyperexcitability and thereby be useful in the therapy of cerebellar ataxia. (clinicaltrials.gov)
  • On this base the investigators published a pilot study in patients with chronic cerebellar ataxia (Ristori et al. (clinicaltrials.gov)
  • The present protocol is aimed at verifying the safety and efficacy of riluzole administration for a longer period, in a larger sample size of patients, with more stringent diagnostic criteria (hereditary cerebellar ataxia), respect to the above pilot study. (clinicaltrials.gov)
  • Efficacy of Riluzole in Hereditary Cerebellar Ataxia: a Randomized Double-blind Placebo-controlled Trial. (clinicaltrials.gov)
  • Clinically, the age of onset is generally around puberty and, as the disease progresses, there is increasing ataxia of the limbs, and eventually most patients are wheelchair bound by the twenties. (clinicaltrials.gov)
  • Cerebellar ataxia (CA) in the Italian Spinone is a serious neurological disease. (aht.org.uk)
  • CLEAR dogs have 2 copies of the normal gene and will neither develop cerebellar ataxia, nor pass a cerebellar ataxia gene to their offspring. (aht.org.uk)
  • CARRIER dogs have one copy of the normal gene and one copy of the mutant gene that causes cerebellar ataxia. (aht.org.uk)
  • They will not develop cerebellar ataxia but will, if bred from, pass on the cerebellar ataxia gene to, on average, 50% of its offspring. (aht.org.uk)
  • AFFECTED dogs have two copies of the mutant gene that causes cerebellar ataxia and will develop the disease. (aht.org.uk)

Paraneoplastic Cerebellar D

  • Autoantibodies directed against the protein encoded by this intronless gene have been found in some patients with paraneoplastic cerebellar degeneration. (genecards.org)
  • Diseases associated with CDR1 include Cerebellar Degeneration and Paraneoplastic Cerebellar Degeneration . (genecards.org)
  • Autoantibodies against CDR1 are found in patients with paraneoplastic cerebellar degeneration. (genecards.org)


  • Cerebellar hypoplasia is the best disease ever. (poetv.com)
  • these people take care of dogs and cats with cerebellar hypoplasia, blind horses. (poetv.com)
  • Are we sure that's not a cerebellar hypoplasia puppy mill? (poetv.com)
  • Cerebellar hypoplasia is just a fancy, city way to say ear mites. (poetv.com)


  • The hereditary cerebellar ataxias include diverse neurodegenerative disorders. (clinicaltrials.gov)
  • Available at: http://www.merckmanuals.com/professional/neurologic-disorders/movement-and-cerebellar-disorders/parkinson-disease. (blakemedicalcenter.com)


  • Molecular basis of cortical-basal ganglia and cortical-cerebellar circuit formation and dysfunction in neurological and psychiatric disease. (upstate.edu)


  • Diseases that affect the structure or function of the cerebellum. (dmoztools.net)


  • The disorder shows an autosomal recessive mode of inheritance: a dog has to inherit two copies of the defective gene (one from each parent) for it to be affected by the disease. (aht.org.uk)
  • CDR1 (Cerebellar Degeneration Related Protein 1) is a Protein Coding gene. (genecards.org)


  • Therefore, it is essential to talk with your doctor about your personal risk factors and/or experience with Parkinson's disease. (blakemedicalcenter.com)
  • What is Parkinson's disease? (blakemedicalcenter.com)
  • Are my symptoms compatible with a diagnosis of Parkinson's disease? (blakemedicalcenter.com)
  • Are my children at risk for Parkinson's disease? (blakemedicalcenter.com)
  • Are there any support groups for people with Parkinson's disease in my community? (blakemedicalcenter.com)
  • What is the usual progression of symptoms in Parkinson's disease? (blakemedicalcenter.com)
  • NINDS Parkinson's disease information page. (blakemedicalcenter.com)
  • Parkinson's disease. (blakemedicalcenter.com)
  • It is possible to develop Parkinson's disease with or without the risk factors listed below. (blakemedicalcenter.com)
  • However, the more risk factors you have, the greater your likelihood of developing Parkinson's disease. (blakemedicalcenter.com)
  • Most people develop Parkinson's disease after the age of 50 (age of onset ranges from 35-85). (blakemedicalcenter.com)
  • It is relatively unusual to develop Parkinson's disease before the age of 40, although it is certainly possible. (blakemedicalcenter.com)
  • Men are about 1.5 times more likely than women to develop Parkinson's disease. (blakemedicalcenter.com)
  • A number of genes have been associated with Parkinson's disease. (blakemedicalcenter.com)
  • Generally, people with these abnormal genes develop Parkinson's disease before the age of 50. (blakemedicalcenter.com)
  • However, the vast majority of Parkinson's disease occurs in older individuals (over the age of 60), and the role of genetics in these individuals is less clear. (blakemedicalcenter.com)
  • Research suggests that blacks and Asians have a slightly lower rate of Parkinson's disease than Caucasians. (blakemedicalcenter.com)
  • Exposure to chemicals, such as herbicides and pesticides, is thought to increase your risk of developing Parkinson's disease. (blakemedicalcenter.com)
  • You also have a greater risk of Parkinson's disease if you live in a rural area, drink well water, or live on a farm. (blakemedicalcenter.com)
  • Epidemiology of Parkinson's disease. (blakemedicalcenter.com)
  • Missing pieces in the Parkinson's disease puzzle. (blakemedicalcenter.com)
  • Systematic review of the risk of Parkinson's disease after mild traumatic brain injury: results of the international collaboration on mild traumatic brain injury prognosis. (blakemedicalcenter.com)
  • In this paper, we describe the methodology to disseminate the adapted tango teaching methods to dance instructor trainees and to implement the adapted tango by the trainees in the community for older adults and individuals with Parkinson's Disease (PD). (jove.com)


  • To date no treatment has been shown to slow progression of the disease and symptomatic therapies are limited to few options that are partially effective. (clinicaltrials.gov)
  • Additional objectives of the study will be the drug's safety and tolerability, and its effect on frataxin, blood vessel reactivity, heart functional indexes, and disease progression. (clinicaltrials.gov)


  • Available at: http://www.aans.org/en/Patient%20Information/Conditions%20and%20Treatments/Parkinsons%20Disease.aspx. (blakemedicalcenter.com)


  • To test the effects of low frequency deep rTMS using the novel HCERMJD-coil on cerebellar deficits in patients with SCA3 and to establish its safety in this population. (clinicaltrials.gov)


  • There is no treatment for the disease, which has an autosomal recessive mode of inheritance. (aht.org.uk)


  • Purkinje cells project inhibitory signals to the deep cerebellar nuclei(DCN) which have a critical role in cerebellar function and motor performance. (clinicaltrials.gov)


  • Zebrafish have become a widely used model organism to investigate the mechanisms that underlie developmental biology and to study human disease pathology due to their considerable degree of genetic conservation with humans. (jove.com)


  • Thus, this protocol provides a feasible strategy that can be implemented by research groups to perform chemical genetics in zebrafish, which can be useful for gaining fundamental insights into developmental processes, disease mechanisms, and to identify novel compounds and signaling pathways that have medically relevant applications. (jove.com)


  • So when are dog breeders just going to give in and start manufacturing dogs with this disease. (poetv.com)
  • Using the information gained from this research, we have developed a linkage-based DNA test for the disease which we estimate will give an accurate result for between 95% and 98% of dogs tested. (aht.org.uk)


  • A risk factor is something that increases your likelihood of getting a disease or condition. (blakemedicalcenter.com)