Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Gait Apraxia”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed2004

Walking difficulties in patients with Alzheimer's disease might originate from gait apraxia.

OBJECTIVES: To investigate whether gait apraxia is a possible cause for some of the walking abnormalities shown by patients with Alzheimer's disease. METHODS: 60 patients with Alzheimer's disease, selected as being free from overt extrapyramidal impairment or other potential causes of walking deficits, were assessed with a new test evaluating aspects of walking and related movements. Norms for this test were collected from a sample of 182 healthy volunteers. RESULTS: 40% of the Alzheimer group performed below the cut off score on this test, and half performed poorly. Performance of the Alzheimer group in the walking skills test correlated highly with scores in a test assessing limb apraxia and with dementia severity. CONCLUSIONS: Gait apraxia may be the cause of walking disorders found in a subgroup of patients with Alzheimer's disease. Its detection is made easier by the use of a standardised test, but still relies heavily on the exclusion of other causes of walking deficits. It is a recognisable and independent form of apraxia.

Adult↗
PubMed1997

[A case of frontal gait apraxia caused by hypoxic encephalopathy].

We reported a rare case who had hypoxic-encephalopathy causing frontal apraxia of gait. The patient, a 34-year-old female, was admitted in July, 1994, complaining of difficulty in walking after anoxic brain damage caused by ventricular arrhythmia. She had difficulty in raising her feet, which appeared to be rooted to the floor. There was no evidence of motor paralysis, spasticity, rigidity or sensory loss, but she did show frontal lobe signs such as foot grasp reflex and Gegenhalten. Cranial MRI showed slight atrophy of the frontal lobe. On T2 weighted image, high-intensity areas were detected at the posterior internal capsule and corona radiata. Single photon emission CT (123I-IMP) demonstrated a low perfusion area which included the inferomedical part of the frontal lobe. After 8 months of hospitalization, her postural instability and unsteady gait slowly improved without treatment as frontal signs such as foot grasp reflex disappeared. We speculate that her apraxia of gait may result from grasp reflex and Gegenhalten.

Adult↗
PubMed1981

Gait apraxia in communicating hydrocephalus.

Apraxia of gait in patients with communicating hydrocephalus appears in the context of a generalised motor disorder that includes defective righting reflexes, generalised increased tone to passive movements, grasp reflexes, difficulty with serial movements of the hands and defective smooth pursuit eye movements. The inability to walk does not appear to be due to a motor disorder but to release of proprioceptive supporting reactions. This mechanism is triggered by proprioceptive stimuli.

Apraxias↗
PubMed2002

Gait apraxia after bilateral supplementary motor area lesion.

OBJECTIVES: The study aimed at addressing the issue of the precise nature of gait apraxia and the cerebral dysfunction responsible for it. METHODS: The case of a patient, affected by a bilateral infarction limited to a portion of the anterior cerebral artery territory is reported. The patient's ability to walk was formally assessed by means of a new standardised test. RESULTS: Due to an anomaly within the anterior cerebral artery system, the patient's lesion was centred on the supplementary motor regions of both hemispheres. He presented with clear signs of gait apraxia that could not be accounted for by paresis or other neurological deficits. No signs of any other form of apraxia were detected. CONCLUSIONS: The clinical profile of the patient and the analysis of 49 cases from previous literature suggest that gait apraxia should be considered a clinical entity in its own right and lesions to the supplementary motor areas are responsible for it.

Apraxias↗
PubMed1998

A SPECT study of patients with gait apraxia without evidence of frontal lobe dysfunction.

BACKGROUND: The pathogenesis of gait apraxia (GA) is unknown. Even though imaging studies provide excellent assessment of brain morphology, there is still a lack of congruous results. Single photon emission computed tomography (SPECT) using Tc-99m hexamethylpropyleneamine oxime (HMPAO) may show alterations in regional cerebral blood flow (rCBF) and provide indirect information about brain metabolism. METHODS: We conducted a SPECT study of GA patients and evaluated the related cortical function. rCBF was assessed in 16 GA patients (15 male, one female; age range 65-79 years, mean 70.5 years) by SPECT using HMPAO. Mean HMPAO cortical or basal ganglia/cerebellum activity ratios were calculated. The regions of interest included the frontal lobe, parietal lobe and basal ganglia. A battery of GA tests and magnetic resonance imaging (MRI) of the brain were also performed in these 16 patients. RESULTS: Nine of the patients had equilibrium disorder, and all 16 patients had locomotion disorder. The MRI findings were lacunar infarct (16/16 in basal ganglia, or 6/16 in thalamus), leukoaraiosis (4/16), enlarged ventricle (3/16), frontal lesion (3/16) and parietal lesion (1/16). Lower rCBF was noted in the frontal lobe (3/16), occipital lobe (1/16, thalamus (7/16) and basal ganglia (9/16). Though SPECT showed decreased rCBF in nine patients (9/16), mean cortical and basal ganglia regional uptake ratios in the patient group were not significantly different from values in the control group (cortical p = 0.0613; basal ganglia p = 0.0576, by Student's t-test). CONCLUSIONS: Though only a small number of patients were studied, it was clear that brain SPECT and MRI did not show any significant abnormalities in the frontal or parietal lobes of patients with GA. Thus, the pathogenesis of GA and its related anatomic lesion should be further investigated.

Aged↗
PubMed1983

Parkinsonism, gait apraxia and dementia associated with intracranial calcifications. A case report.

A 52-year-old Black man with therapy-resistant parkinsonism, gait apraxia and dementia but no endocrine abnormality was found to have extensive intracerebral calcifications which included the basal ganglia. Although most patients with radiological evidence of calcifications in the basal ganglia remain asymptomatic, a small group may present with an extrapyramidal syndrome that is usually progressive, resistant to therapy, and not associated with an endocrine disorder. Plain skull radiography and computed tomography should therefore be performed in patients presenting with a parkinsonian syndrome unresponsive to therapy.

Ataxia↗
PubMed1989

Risk factors for the syndrome of ventricular enlargement with gait apraxia (idiopathic normal pressure hydrocephalus): a case-control study.

A case-control study was performed to verify the association between the risk factors for cerebrovascular disease and the syndrome of ventricular enlargement with gait apraxia (VEGAS). This syndrome was defined on the basis of clinical and CT criteria alone; however, it may be representative of patients with idiopathic normal pressure hydrocephalus in whom gait disturbance is the initial symptom. Seventeen patients were matched for age and sex with one hospitalised and two general population controls. Among the risk factors considered we found a significant statistical association between VEGAS and hypertension (odds ratio = 3.14; p = 0.032), ischaemic heart disease (odds ratio = 4.20; p = 0.013), ECG ischaemic changes (odds ratio = 3.67; p = 0.029), low HDL-cholesterol levels (odds ratio = 3.75; p = 0.028) and diabetes (odds ratio = 6.00; p = 0.018). Our findings indicate that risk factors for cerebrovascular disease may play a role in the development of VEGAS.

Aged↗
PubMed1985

Gait apraxia in normal-pressure hydrocephalus: patterns of movement and muscle activation.

We made gait recordings in 11 patients with normal-pressure hydrocephalus. Sagittal rotations in hip, knee, and ankle joints were determined with intermittent light photography or with polarized light goniometry. In eight patients, gait muscle activation was determined with integrated surface EMG from six leg muscles on one side. We assessed the patterns of movement and muscle activity by averaging data from 20 gait cycles. Reduced speed and range of movements, short steps, small foot-floor clearance, and low swing-to-stance ratio were typical. The activation of the calf muscles was regularly premature and low. In severe disorders, there was continuous activity in the antigravity muscles acting on hip and knee joints. Gait records verified improvement after CSF drainage or shunting.

Aged↗
PubMed1989

L-threo-3,4-dihydroxyphenylserine treatment for gait apraxia in parkinsonian patients.

L-threo-3,4-dihydroxyphenylserine (L-DOPS) was administered to six parkinsonian patients for the treatment of gait related akinesia which was refractile to L-DOPA treatment. One responded with marked improvement and one with only mild improvement. Although number of patients who respond markedly to this noradrenaline precursor, L-DOPS, is limited, L-DOPS was felt to be the most effective treatment modality for L-DOPA refractile gait related akinesia and L-DOPA related orthostatic hypotension.

Aged↗
PubMedDate not supplied

[Apraxia of gait: an acquired sequela with a poor prognosis].

INTRODUCTION: Gait apraxia is not used to be considered as a diagnostic entity in Pediatric Neurology. CASE REPORTS: We present two pediatric patients that, after to have acquired normal gait and in consequence of a acute process, they lost the capacity to walk. In spite of intensive rehabilitation treatment hold along various years, they had not been able to help them. Both injury were very dissimilar; in one of them was affected the precentral and paracentral cortex in consequence of an encephalitic process. In the other, the basal ganglia and the hippocampus after a situation of near-drowning at the age of 15 months. CONCLUSION: The mechanism of this disorder is discussed and emphasis is done in its badly long-term prognosis.

Brain Diseases↗
PubMed1992

Cortico-basal ganglionic degeneration. A case report.

The case of a Brazilian patient with cortico-basal ganglionic degeneration (CBGD) is presented. Since three years ago, a 71-year old male displays asymmetric ideomotor apraxia, gait apraxia, cortical sensory impairment, myoclonus, limp dystonia and rigidity. His mental status is spared. There is neither consanguinity nor similar cases in his family. The differential diagnosis of CBGD is discussed. A brief review of the literature is made stressing the clinical and pathological features of CBGD. This disease is poorly known and probably underdiagnosed. Its diagnosis can be safely made based on clinical grounds.

Aged↗
PubMed1993

[Apraxia of gait and disorders in posture and locomotion].

Apraxia of gait is a unique disorder of locomotion characterized by inability in lifting the feet from the floor despite alternating stepping action (frozen gait), and disequilibrium. Responsible site of lesions are in the frontal lobe and/or the basal ganglia. It is observed in an advanced stage of Parkinson's (PD) or vascular parkinsonism with multiple cerebral infarction (MCI). Studies on equilibrium and natural gait have disclosed unique features in this condition. Records of floor reaction forces in forward locomotion showed that vertical-foreaft vector angles at kick-off phase is small in both PD and MCI with frozen gait. EMG of antagonists in leg muscles were either reciprocal or coincided in frozen gait, and rhythm of stepping was crucial for development of freezing. Center of foot pressure (CFP) in forward-bent natural posture in PD still locates behind that of normals. For voluntary forward bending, maximal shift of CFP was smaller, and increase in EMG was larger in PD subjects. Pushing chest backward results in step-out or fall in parkinsonians. In this response, EMG in the pretibial muscles were the same amount in both PD and normals. However, velocity in hip extension and amount of knee and ankle displacement were smaller in PD.

Apraxias↗
PubMed1989

[Clinical and physiological study of apraxia of gait and frozen gait].

A study of clinical features and an analysis of gait with floor reaction forces and EMG of leg flexors and extensors were made in patients with multiple cerebral infarction or patients with Parkinson's disease having frozen gait. A case with occlusion of the bilateral anterior cerebral arteries resulting in massive infarction of the infero-medial part of the frontal lobes was also studied as he showed a unique disorder characterized by apraxia of gait. Frozen gait is characterized by shuffling steps, broad-based stance, positive foot grasp, kinesia paradoxa and disturbance of postural reflexes. The vector angle which shows foot pressure in forward locomotion was decreased in patients with frozen gait. EMGs of lower leg muscles in frozen gait were grouping of potentials corresponding to the shuffle and reciprocity between flexors and extensors was preserved. The patient with infarction of the bilateral anterior cerebral arteries showed a peculiar disorder of gait which was characterized by an inability to initiate stepping. It is considered as "apraxia of gait" in a classical sense, which differs from frozen gait. Observation of this patient suggests that the infero-medical part of the frontal lobe plays an important role in the initiation of gait. Furthermore, common features of frozen gait in patients with Parkinson's disease and in patients with multiple cerebral infarction involving the frontal lobe suggest that the nigrostriatal structures and the frontal lobe are important in CNS mechanisms subserving smooth locomotion.

Aged↗