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Gait Disturbance (gait + disturbance)
Selected AbstractsGait disturbance interpreted as cerebellar ataxia after MMR vaccination at 15 months of age: a follow-up studyACTA PAEDIATRICA, Issue 1 2000A-M Plesner Measles, mumps and rubella (MMR) vaccination was included in the Danish childhood vaccination programme in 1987. During the following 10-y period, 550 notification records of adverse events after MMR vaccination at 15 mo of age have been registered, and a total of 41 notifications have included "gait disturbance". This corresponds to a frequency of 8 per 100 000 doses of MMR vaccine used for 15-mo-old children. The symptoms and signs are characteristic of cerebellar ataxia. In 28 notifications, the descriptions by the doctors included only "gait disturbance", while in 13 an additional interpretation was included. Thirty-two parents (78%) filled in a questionnaire and 26 (63%) agreed to participate in a clinical follow-up study. The gait disturbance symptoms mainly occurred 7,14 d after the vaccination, and the duration was median 1,2 wk (range 1 d to more than 4 mo). One-third of the children had symptoms lasting more than 2 wk. Significantly more children with long duration of symptoms had some kind of complaint or clinical signs at the follow-up in 1997. Gait disturbance registered after MMR vaccination seems to be more frequent than hitherto reported. Most cases are mild and short-lasting and a longer duration of symptoms seems to be predictive of late sequelae. A clinical diagnosis of cerebellar ataxia after MMR and the exact frequency of this adverse event remains to be tested in prospective studies. [source] The power of cueing to circumvent dopamine deficits: A review of physical therapy treatment of gait disturbances in Parkinson's diseaseMOVEMENT DISORDERS, Issue 6 2002Tamar C. Rubinstein MSc Abstract Gait disturbances are among the primary symptoms of Parkinson's disease (PD) and contribute significantly to a patient's loss of function and independence. Standard treatment includes antiparkinsonian drugs, primarily levodopa. In addition to the standard drug regime, physical therapy is often prescribed to help manage the disease. In recent years, there have been promising reports of physical therapy programs combined with various types of sensory cueing for PD. In this brief review of the literature, we summarize the evidence regarding the clinical efficacy of different physical therapy programs for PD, specifically with respect to improving gait. We also discuss the potential therapeutic mechanisms of sensory cueing and review the studies that have used cueing in the treatment of gait in PD. This review of the literature shows two key findings: (1) despite its relatively long history, the evidence supporting the efficacy of conventional physical therapy for treatment of gait in PD is not strong; and (2) although further investigation is needed, sensory cueing appears to be a powerful means of improving gait in PD. © 2002 Movement Disorder Society [source] Gait disturbances in patients with schizophrenia and adaptation to treadmill walkingPSYCHIATRY AND CLINICAL NEUROSCIENCES, Issue 3 2005ALBERT PUTZHAMMER md Abstract, This study evaluated the gait patterns of schizophrenic patients at free gait and at three fixed velocities on a treadmill. The effects of illness and antipsychotic treatment on gait parameters and on adaptation to treadmill walking were compared. Gait parameters of 14 drug-naïve schizophrenic patients, 14 patients treated with conventional antipsychotics, 14 patients treated with olanzapine, as well as 14 matched controls were assessed on a walkway and on a treadmill at three different velocities (very slow, intermediately slow, and comfortable) using an ultrasonic movement analysis system. At free gait, all patients showed a significantly decreased gait velocity, predominantly due to a shorter stride length, when compared to the controls, with the most striking difference observed between the patients treated with conventional neuroleptics and the controls (anova, P , 0.001). Cadence (steps per second) did not differ between the investigated groups. When gait was evaluated on the treadmill, differences in stride length and cadence were significant only at the very slow treadmill velocity (anova, P , 0.05). In all patient groups, mean stride length was decreased and cadence compensationally increased. Significant differences between the patient groups were no longer detectable. With increasing treadmill velocities, gait parameters of all patient groups normalized. The results show that, like in patients with Parkinson's Disease, impaired gait parameters can also be normalized in schizophrenic patients by external stimulation via treadmill walking. [source] Gait disturbance interpreted as cerebellar ataxia after MMR vaccination at 15 months of age: a follow-up studyACTA PAEDIATRICA, Issue 1 2000A-M Plesner Measles, mumps and rubella (MMR) vaccination was included in the Danish childhood vaccination programme in 1987. During the following 10-y period, 550 notification records of adverse events after MMR vaccination at 15 mo of age have been registered, and a total of 41 notifications have included "gait disturbance". This corresponds to a frequency of 8 per 100 000 doses of MMR vaccine used for 15-mo-old children. The symptoms and signs are characteristic of cerebellar ataxia. In 28 notifications, the descriptions by the doctors included only "gait disturbance", while in 13 an additional interpretation was included. Thirty-two parents (78%) filled in a questionnaire and 26 (63%) agreed to participate in a clinical follow-up study. The gait disturbance symptoms mainly occurred 7,14 d after the vaccination, and the duration was median 1,2 wk (range 1 d to more than 4 mo). One-third of the children had symptoms lasting more than 2 wk. Significantly more children with long duration of symptoms had some kind of complaint or clinical signs at the follow-up in 1997. Gait disturbance registered after MMR vaccination seems to be more frequent than hitherto reported. Most cases are mild and short-lasting and a longer duration of symptoms seems to be predictive of late sequelae. A clinical diagnosis of cerebellar ataxia after MMR and the exact frequency of this adverse event remains to be tested in prospective studies. [source] Donor site morbidity after harvesting of proximal tibia boneHEAD & NECK: JOURNAL FOR THE SCIENCES & SPECIALTIES OF THE HEAD AND NECK, Issue 6 2006Yuan-Chien Chen DDS Abstract Background. Bone-grafting procedures are common in head and neck surgery. Donor site morbidity is an important factor in deciding the site for harvest of cancellous bone. The tibia has been recommended as a harvest site. Use of the proximal tibia as a donor site is associated with few complications. Our present study used proximal tibia bone grafts to reconstruct maxillofacial defects and augment bone volume for implantation. Methods. A retrospective study was undertaken to analyze 40 proximal tibia bone grafts in maxillofacial reconstruction. Minimal follow-up was 6 months. Results. There were no major complications during the follow-up period. Early minor complications (15%) included temporary sensory loss and ecchymosis. Late minor complication (2.5%) was gait disturbance for 2 months. Long-term minor complication (2.5%) was an unsightly scar. Conclusion. The procedure for proximal tibia bone graft is easy, has less operative risk, and results in a lower postoperative morbidity rate. Based on our findings, we believe the proximal tibia offers a reliable site for harvest of sufficient quantities of good-quality cancellous bone. © 2006 Wiley Periodicals, Inc. Head Neck 28:496,500, 2006 [source] Ipsilateral Hemiplegia in a Lateral Medullary Infarct, Opalski's SyndromeJOURNAL OF NEUROIMAGING, Issue 1 2003Yasuyuki Kimura MD ABSTRACT A 42-year-old man was admitted complaining of the sudden onset of headache, vomiting, vertigo, and gait disturbance. The authors found hemiparesis of his right limbs, right Horner's syndrome, and decreased pain and temperature sensation of his right face and left limbs. Diffusion-weighted imaging (DWI) showed an acute small infarct located on the right side of the lateral lower medulla. This is the first report of Opalski's syndrome with lower medullary infarction detected by DWI. [source] A child with Miller Fisher syndromeJOURNAL OF PAEDIATRICS AND CHILD HEALTH, Issue 4 2002J Garrett Abstract: We describe the case of a six-year-old girl who presented with a 3-day history of diplopia and gait disturbance following a febrile flu-like illness. On examination she was found to have ataxia, areflexia and ophthalmoplegia, and a diagnosis of Miller Fisher syndrome was made after the exclusion of other conditions. This report outlines the frequency of Miller Fisher syndrome and lists the differential diagnoses that should be considered in Australia. In addition, the occurrence of pupillary dysfunction is discussed. [source] Abstracts of the 8th Meeting of the Italian Peripheral Nerve Study Group: 83JOURNAL OF THE PERIPHERAL NERVOUS SYSTEM, Issue 1 2003G Lauria We describe a 64-year-old patient complaining of progressive gait disturbance, referred to the compressive effect of multiple discal protrusions, for about 3 years. At the age of 62 he presented epileptic seizures during a febrile episode. Cerebral MRI showed bilateral frontobasal T2-weighted hyperintensity involving cortex and white matter. Partial seizures reappeared one year later and a MRI revealed a mild frontobasal atrophy. At the moment of our observation, neurological examination showed waddling gait with bilateral foot drop, muscular atrophy and weakness limited to the gluteal muscles and widespread deep tendon areflexia. Nerve conduction studies showed absent F-waves at both upper and lower limb examination, with normal distal sensorimotor nerve conduction. Needle EMG examination detected mild chronic partial denervation, predominant in proximal muscles of lower limbs. Somatosensory evoked potentials recorded from upper extremities showed bilateral increase in early latencies (N9). Overall, neurophysiological findings indicated a widespread radiculopathy. Serum exams revealed positive anti-nucleus (1:640, granular). CSF examination detected increased IgG level and several oligoclonal bands. Chest radiogram was normal. Soon after our first observation, the patient showed symptoms of respiratory insufficiency. A CT scans revealed a thoracic mass compatible with microcytoma, whereas anti-Hu (3 +) antibodies and increased NSE (neuronal specific enolase) titer were found. In the following two weeks, the patient showed a progressive worsening of the general clinical conditions and died. We interpreted this complex neurological picture, which included an atypical limbic encephalitis and a slowly progressive polyradiculopathy, as a paraneoplastic syndrome. The almost complete resolution of the encephalitic process and the subtle chronic involvement of the peripheral nervous system, characterized by a limited, though widespread, radicular impairment, are rather peculiar features. [source] Parkinsonism and dystonia caused by the illicit use of ephedrone,A longitudinal study,MOVEMENT DISORDERS, Issue 15 2008Marianna Selikhova MD Abstract A neurological syndrome characterized by levodopa unresponsive bradykinesia, retropulsion with falls backwards, dysarthria, gait disturbance, dystonia, and emotional lability was identified in 13 male opiate addicts following the prolonged intravenous use of ephedrone (methcathinone), a central nervous stimulant prepared from pseudoephedrine, potassium permanganate, and vinegar. The natural history, response to treatment, and clinical features has been studied, and MR and dopamine transporter SPECT brain imaging were carried out. Pubic hair was sampled for manganese. The clinical and radiological picture closely resembled previous reports of chronic manganese poisoning and increased mean manganese level in pubic hair observed for at least 1 year after cessation of ephedrone. Odor identification was intact. Cognitive assessment showed a mild executive dysfunction and a mild depression. DaTSCANs were all normal. The neurological syndrome bears some similarities to PSP but differs from Parkinson's disease. Delayed neurological progression despite discontinuation of ephedrone occurred in one-third of cases. Ephedrone poisoning should be considered as a possible cause of secondary Parkinsonism in young adults, particularly from Eastern Europe. © 2008 Movement Disorder Society [source] 69-Year-old man with gait disturbance and parkinsonism,MOVEMENT DISORDERS, Issue 3 2001Connie Marras MD [source] Progressive supranuclear palsy combined with Alzheimer's disease: A clinicopathological study of two autopsy casesNEUROPATHOLOGY, Issue 3 2009Rieko Sakamoto We present here the clinicopathological characteristics of two autopsy-confirmed cases comorbid of progressive supranuclear palsy (PSP) and Alzheimer's disease (AD). Histopathologically, the amount and distribution of neurofibrillary tangles (NFTs) in the basal ganglia and brainstem fulfilled the pathological criteria of PSP proposed by the National Institute of Neurological Disorders and Stroke , The Society for PSP (NINDS-SPSP). The Braak stages of senile plaques and NFTs were stage C and stage V in Case 1, and stage C and stage IV in Case 2. These neuropathological findings confirmed that the two patients had combined PSP with AD. Our patients presented clinically with executive dysfunction prior to memory disturbance as an early symptom. Not only neurological symptoms such as gait disturbance, supranuclear ophthalmoplegia and pseudobulbar palsy, but emotional and personality changes and delirium were prominent. Therefore, symptoms of subcortical dementia of PSP were more predominant than AD-related symptoms in the present two patients. Comorbid PSP and AD further complicates the clinical picture and makes clinical diagnosis even more difficult. [source] Venous congestive myelopathy of the cervical spinal cord: An autopsy case showing a rapidly progressive clinical courseNEUROPATHOLOGY, Issue 3 2007Akio Kimura We report a rapidly progressive myelopathy in a 74-year-old Japanese man who was admitted to our hospital with a 4-month history of progressive gait disturbance and died of pneumonia followed by respiratory failure on the 22nd day of admission. During the course of his illness, magnetic resonance imaging (MRI) revealed intramedullary lesions with edematous swelling from the medulla oblongata to the spinal cord at the level of the fourth vertebra. After administration of contrast medium, the ventral portion of the lesion was mildly and irregularly enhanced and a dilated vessel was recognized along the ventral surface of the upper cervical cord. At autopsy, ischemic changes were observed in the upper-to-middle cervical cord segments, with so-called arterialized veins in the subarachnoid space. No neoplastic lesions were found within or outside the brain and spinal cord. These pathological findings were essentially those of venous congestive myelopathy (VCM) associated with dural arteriovenous fistulae (AVF), formerly known as Foix,Alajouanine syndrome. VCM associated with dural AVF, which is now considered to be treatable in the early stages, is rare found in the cervical spinal cord. The present autopsy case, with MRI findings, provides further information that might be useful for recognition and diagnosis. [source] Clear cell ependymoma of the fourth ventricleNEUROPATHOLOGY, Issue 4 2004Masahito Katoh Two cases of clear cell ependymoma (CCE) of the fourth ventricle are reported in a 49-year-old woman with dysphagia and a 59-year-old woman with dizziness and gait disturbance. CCE is a relatively new variant of ependymoma added to the WHO classification of tumors in 1993. Tumor cells display an oligodendroglioma-like appearance with a clear perinuclear halo. Most infratentorial CCE tumors are located in the cerebellum. There are only three cases, including the present two cases, that have been reported to affect the fourth ventricle. [source] Extracranially extended meningothelial meningiomas with a high MIB-1 index: A report of two casesNEUROPATHOLOGY, Issue 1 2004Shoko M. Yamada Meningiomas that extend from the meninges to the extracranial tissue and result in skull osteolysis have been known to take an aggressive clinical course. Two such cases in elderly patients are reported. Case 1 is an 82-year-old woman who had undergone removal of the parasagittal meningioma (meningothelial meningioma with 5% of MIB-1 index) 4 years and 6 months previously, developed recurrence of the tumor that extended to extracranial soft tissue. Biopsy obtained from the subcutaneous tissue showed an atypical meningothelial meningioma with 20% of MIB-1 index. In case 2 an 84-year-old man, who developed rapidly progressing dementia and gait disturbance, the MRI study revealed an intracranial-extraaxial right frontal tumor with an extracranial extension resulting in skull osteolysis. Pathological examination of the totally resected tumor identified meningothelial meningioma, but MIB-1 index of the intracranial portion of the tumor was less than 0.1%, while that of the extracranial portion was approximately 15%. Although the meningiomas presently reported failed to show histological features of malignancy, the high MIB-1 index indicated that they were rapidly growing tumors. In the present report it is considered that meningioma cells that invade the skull and extracranial tissue are biologically aggressive and require total resection, as long as the condition of the patients is feasible for surgery. [source] Abnormal somatosensory evoked potentials in two patients with conversion disorderPSYCHIATRY AND CLINICAL NEUROSCIENCES, Issue 2 2004KAZIM M. YAZICI md Abstract, On clinical grounds, somatosensory evoked potentials (SEP) and motor evoked potentials (MEP) are currently used to discriminate between hysterical and neurological conditions. The present paper reports on two patients with severe gait disturbance who had the near-total absence of SEP responses on the scalp during the symptomatic period, which normalized after recovery. These findings, along with others, may shed light on the brain correlates of conversion phenomena. [source] Parkinsonian signs and substantia nigra neuron density in decendents elders without PD,ANNALS OF NEUROLOGY, Issue 4 2004G. Webster Ross MD Substantia nigra (SN) neurons were counted on single, transverse caudal midbrain sections from 217 male participants in the Honolulu-Asia Aging Study, aged 74,97 years at death. Quadrants areas within the SN were determined with a planimeter and neuronal density was expressed as neurons/mm2 for 10 Parkinson's disease (PD) cases, 29 incidental Lewy body cases, and 178 controls with neither condition. Mean densities in all quadrants were significantly lower in the PD group compared with the other groups (p = 0.006). This relationship was strongest in the ventrolateral quadrant. In a subgroup of 50 controls who were examined with the Unified Parkinson's Disease Rating Scale an average of 2.1 years prior to death, there was an association of stooped posture (p = 0.009), postural instability (p = 0.013), body bradykinesia (p = 0.048), and gait disturbance (p = 0.05) with neuron density in the dorsolateral quadrant; and impaired speech (p = 0.014), abnormal facial expression (p = 0.022), and difficulty rising from a chair (p = 0.032) with neuron density in the dorsomedial quadrant. There was a significant association of increasing number of signs present with decreasing neuron density in both quadrants (p = 0.001 for trend). Low SN neuron density may be the basis for parkinsonian signs in the elderly without PD. Ann Neurol 2004 [source] White matter changes in normal pressure hydrocephalus and Binswanger disease: specificity, predictive value and correlations to axonal degeneration and demyelinationACTA NEUROLOGICA SCANDINAVICA, Issue 6 2002M. Tullberg Objectives, To analyse the diagnostic and prognostic value of periventricular hyperintensity (PVH) and deep white matter hyperintensity (DWMH) magnetic resonance imaging (MRI) changes and their relation to symptoms and cerebrospinal fluid (CSF) markers of demyelination (sulphatide) and axonal degeneration [neurofilament triplet protein (NFL)] in a large series of patients with normal pressure hydrocephalus (NPH) and Binswanger disease (BD). Materials and methods, PVH and DWMH were determined by a semi-automatic segmentation method on T2-weighted images in 29 patients with NPH and 17 patients with BD. CSF analyses, psychometric testing and quantification of balance, gait and continence were performed in all patients and also postoperatively in NPH patients. Results, No MRI variable could identify NPH or BD patients. Abundant PVH and DWMH preoperatively correlated with improvement in gait, balance and psychometric performance after shunt surgery (P < 0.05). CSF sulphatide correlated positively with the amount of DWMH (P < 0.05) while NFL was correlated to both PVH and DWMH (P < 0.05). Abundant PVH correlated with poor psychometric performance while DWMH correlated with gait disturbance (P < 0.05). Postoperative reduction in PVH correlated with improvement in gait, balance and psychometric performance. Conclusion, In spite of a refined quantification method, NPH and BD patients exhibited similar MRI changes. MRI had a predictive value in NPH patients. DWMH might relate to demyelination and PVH to neuronal axonal dysfunction. NPH and BD share the major part of symptoms and MRI changes, indicating a common pathophysiological pattern, and we raise the question of how to treat BD patients. [source] PAINFUL NEUROPATHY, MONOCLONAL GAMMOPATHY AND AMYLOID DEPOSITS: RESPONSE TO THERAPY IN 3 CASESJOURNAL OF THE PERIPHERAL NERVOUS SYSTEM, Issue 1 2002Article first published online: 11 MAR 200 Siciliano G.1, D'Avino C.1, Panichi V.2, Azzarà A.3, Del Corona A.1, Pollina L.3, Murri L.1 1Department of Neuroscience, 2Department of Internal Medicine and 3Department of Oncology,University of Pisa-Italy Amyloidosis is a systemic disease with a wide organic involvement. Amyloidotic polyneuropathies may be genetic in their origin or present in association with a number of chronic inflammatory dysimmune disorders. We report on three patients affected by predominantly sensitive polyneuropathy, monoclonal gammopathy and amyloidosis. Patient 1. Woman, 72 years old, with a one year history of painful paraesthesias, ataxic gait and demyelinating predominantly sensitive polyneuropathy at 4 limbs also with involvement of sympathetic fibres. Blood protein electrophoresis showed a monoclonal gammopahty (IgG-k) with normal bone marrow biopsy and positivity for amyloid at fat biopsy. The patient has been treated with melphalan 0.2 mg/Kg/day+prednisone 100 mg/day for 7 days each month for 6 months with good efficacy and only a transient reduction in platelet and white blood cells count. Patient 2. Man, 60 years old, new diagnosis of diabetes with a 9 month history of painful paraesthesias and hyposthenia, a demyelinating sensory-motor polyneuropathy at 4 limbs. The patient presented an IgG-, monoclonal gammopathy with normal bone marrow biopsy, fat biopsy but not sural nerve biopsy positive for amyloid. The patient underwent melphalan+prednisone therapy, with insulinic control of glycemia. He presented a clear-cut improvement in sensitive-motor symptomatology. Patient 3. Man, 72 years old, with a 15 year history of ulcerous rectocolites. Since 1998 started complaining of paraesthesias and disaesthesias at four limbs associated with gait disturbances. The patient presented an IgG-, monoclonal gammopathy with normal bone marrow aspiration and elevated serum Interleukin-6 levels, fat biopsy positive for amyloid, and high anti-MAG antibodies titer (1:100000). Because of RCU, melphalan therapy was excluded and the patient is at the moment under fludarabine (25 mg/m2/day) ev for 5 days each 6 weeks for 6 bouts. [source] AUTOMIC FAILURE AND NORMAL PRESSURE HYDROCEPHALUS IN A PATIENT WITH CHRONIC DEMYELINATING INFLAMMATORY NEUROPATHYJOURNAL OF THE PERIPHERAL NERVOUS SYSTEM, Issue 1 2002M. Laurà A 75-year-old man with HCV hepatitis developed at the age of 70 presented with rest and action tremor localized at both hands and progressive cognitive impairment with memory loss. Four years later he begun to complain of progressive fatigue, occasional falls, numbness at the extremities and orthostatic hypotension. One month after admission, he rapidly worsened with inability to walk, mainly because of autonomic failure. Neurological examination revealed gait disturbances, including a wide base of support and short stride, slurred speech, reduction of upward gaze, rest and action tremor at both hands, intrinsic hand muscle and anterior tibialis muscle wasting and weakness on both sides, absent deep tendon reflexes, loss of vibration sense at lower limbs, and bilateral pes cavus. Routine laboratory studies, autoantibodies, thyroid function, neoplastic markers and immunoelectrophoresis were normal. Cryoglobulins were absent, whereas CSF protein content was increased (142 mg/dl). Autonomic nervous system investigation detected severe orthostatic hypotension. Nerve conduction studies showed absent sensory potentials and a marked reduction of compound motor action potential amplitudes and of motor conduction velocities. A sural nerve biopsy revealed remarkable onion bulb-like changes, endoneurial and perivascular infiltrations of inflammatory cells. Psychometric tests showed mild cognitive impairment. Brain MRI was consistent with normotensive hydrocephalus. The findings indicated the presence of chronic inflammatory demyelinating polyneuropathy, autonomic nervous system involvement and normal pressure hydrocephalus. A condition of multiple system atrophy (MSA) might be taken into account, even if somatic peripheral nerve involvement may rarely occur in MSA. Moreover the normal pressure hydrocephalus could be due to the high protein content in CSF (Fukatsu R et al., 1997). [source] REM sleep behavior disorder is not linked to postural instability and gait dysfunction in Parkinson,MOVEMENT DISORDERS, Issue 11 2010David H. Benninger MD Abstract To evaluate a potential association of REM-sleep behavior disorder (RBD) with gait and postural impairment in Parkinson's disease (PD). Gait difficulties and postural impairment are frequent in PD and are a major cause of disability. Animal studies indicate a key role of the pedunculopontine nucleus (PPN) in gait, postural control, and REM sleep, and also in the pathophysiology of RBD. In humans, such an association has not been investigated. Twenty-six patients with mild-to-moderate PD (13 with polysomnography confirmed and 13 with excluded RBD), and 20 age-matched healthy controls were prospectively investigated. Gait assessment on a treadmill, and static and dynamic posturography were performed. PD patients with RBD do not differ from those without RBD in gait and postural control. Greater severity of PD or prevalence of gait and postural disturbances in the presence of RBD were not found. RBD was not associated with any particular motor phenotype. We found no association of RBD with gait disturbances and postural impairment. Human gait and postural control and RBD appear to depend upon different neuronal circuits. © 2010 Movement Disorder Society [source] Basal ganglia physiology and deep brain stimulation,MOVEMENT DISORDERS, Issue S1 2010Andres M. Lozano FRCSC Abstract Despite improvements in anatomic imaging of the basal ganglia, microelectrode recording is still an invaluable tool in locating appropriate targets for neurosurgical intervention. These recording also provide an unparalleled opportunity to study the pathophysiological aspects of diseases. This article reviews the principles of microelectrode recording in functional neurosurgery and discusses the pathologic neurophysiologic findings commonly encountered. It also highlights some of the potential mechanisms of action of both dopaminergic drugs and deep brain stimulation. In addition we review the recent work on pedunculopontine nucleus neurophysiology and trials of deep brain stimulation in that region for gait disturbances in Parkinson's disease. © 2010 Movement Disorder Society [source] The power of cueing to circumvent dopamine deficits: A review of physical therapy treatment of gait disturbances in Parkinson's diseaseMOVEMENT DISORDERS, Issue 6 2002Tamar C. Rubinstein MSc Abstract Gait disturbances are among the primary symptoms of Parkinson's disease (PD) and contribute significantly to a patient's loss of function and independence. Standard treatment includes antiparkinsonian drugs, primarily levodopa. In addition to the standard drug regime, physical therapy is often prescribed to help manage the disease. In recent years, there have been promising reports of physical therapy programs combined with various types of sensory cueing for PD. In this brief review of the literature, we summarize the evidence regarding the clinical efficacy of different physical therapy programs for PD, specifically with respect to improving gait. We also discuss the potential therapeutic mechanisms of sensory cueing and review the studies that have used cueing in the treatment of gait in PD. This review of the literature shows two key findings: (1) despite its relatively long history, the evidence supporting the efficacy of conventional physical therapy for treatment of gait in PD is not strong; and (2) although further investigation is needed, sensory cueing appears to be a powerful means of improving gait in PD. © 2002 Movement Disorder Society [source] Molecular and clinical consequences of novel mutations in the arylsulfatase A geneCLINICAL GENETICS, Issue 1 2009ugowska Metachromatic leukodystrophy (MLD), a severe neurodegenerative metabolic disorder, is caused by deficient activity of arylsulfatase A (ARSA; EC 3.1.6.8), which leads to a progressive demyelinating process in central and peripheral nervous systems. In this study, a DNA sequence analysis was performed on six Polish patients with different types of MLD. Six novel mutations were identified: one nonsense (p.R114X), three missense (p.G122C, p.G293C, p.C493F) and two frameshift mutations (g.445_446dupG and g.2590_2591dupC). Substitutions p.G293C and p.C493F and duplication g.445_446dupG caused a severe reduction of enzyme activity in transient transfection experiments on mammalian cells (less than 1% of wild-type (WT) ARSA activity). Duplication 2590_2591dupC preserved low-residual ARSA activity (10% of WT ARSA). In summary, the novel MLD-causing mutations in the exons 2, 5 and even in 8 of the ARSA gene described here can be classified as severe type 0, leading in homozygosity to the late infantile form MLD. Growth retardation, delayed motor development, gait disturbances, tonic,clonic seizures and non-epileptic muscle spasms were the first onset symptoms in patients with late infantile form of MLD. In individual with juvenile type MLD gait disturbances evidenced the onset of the disease, while in a patient with late juvenile MLD, difficulties at school were displayed. [source] | ||||||||||||||||||||||