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Movement disorders
Published in Henry J. Woodford, Essential Geriatrics, 2022
The neuropathological findings of DLB include Lewy bodies, which are spherical, eosinophilic, intracytoplasmic inclusion bodies composed of alpha-synuclein protein. They may be found throughout the brain but appear more commonly in the basal ganglia and limbic system. Standardised diagnostic criteria are available for DLB.98 Diagnosis typically requires dementia plus two or more of the key clinical features as listed above. Parkinsonism eventual appears in over 85% of people with DLB.98 Resting tremor is uncommon. Shuffling gait and impaired motor initiation are likely. Visual hallucinations occur in around 80%. Diagnostic accuracy remains challenging. It is estimated that around 20% of DLB diagnoses are incorrect when compared to autopsy cerebral pathological findings.99
Distribution
Published in Kerry Layne, Albert Ferro, Janice Rymer, 100 Cases in Clinical Pharmacology, Therapeutics and Prescribing, 2020
The patient is alert and orientated to time, place and person. He has no visible injuries. Cardiovascular, respiratory and abdominal system examinations are unremarkable. Neurological examination identifies bilateral increased tone in the upper limbs with a pronounced resting tremor, consistent with ‘cogwheel rigidity’. There is a slow, rhythmic ‘pill-rolling’ tremor in the left hand. The patient’s face appears expressionless, or ‘mask-like’ and his speech is monotonous. He walks with a shuffling gait.
Clinical examination
Published in Nicholas Summerton, Primary Care Diagnostics, 2018
Nowadays in many family/general practices patients are summoned into the consulting room by means of electronic boards, loudspeakers or receptionists. In other more traditional set ups the doctor walks into the waiting room and invites the patient in. If we are going to practise primary care diagnostics I would argue that it is important to appreciate that the ‘clinical examination’ commences from the moment we clap eyes on the patient. If we simply sit immobile in our consulting rooms we might easily miss the difficulty a patient with polymyalgia rheumatica can have rising from the waiting room chair. Observation of the patient’s gait as they walk down the corridor can provide important information on neurological or musculoskeletal problems. In one study of the diagnosis of Parkinson’s disease, a shuffling gait provided a positive likelihood ratio of 3.3, difficulty rising from a chair 1.9, whereas tremor only added 1.4.6 Emotions can also affect walking; some depressed patients have a characteristic gait, marked by a shorter stride and weaker push-off with the heel when compared with non-depressed individuals.7
Spinal cord stimulation for gait disturbances in Parkinson’s disease
Published in Expert Review of Neurotherapeutics, 2023
Nora Vanegas-Arroyave, Joseph Jankovic
Parkinson’s disease (PD) is the second most common neurodegenerative disorder after Alzheimer’s disease, with an estimated number of 1.2 million cases in North America by 2030 [1]. In addition to tremor, bradykinesia, and rigidity, PD patients exhibit a variety of other motor symptoms including shuffling gait, postural instability and freezing of gait (FOG) [2–6]. The latter is characterized by transient periods during which the individual is unable to produce effective steps when initiating gait (start hesitation), moving through narrow passages, or turning, often described by the patient as ‘the feet are stuck to the floor’ [7,8]. Compared to non-freezers, PD patients with FOG have longer disease duration, more severe motor fluctuations, take higher doses of dopaminergic agents, and are more likely to exhibit cognitive impairment [4]. Phenotypically, the vast majority of patients with FOG (89%) belong to the postural-instability-gait difficulty (PIGD) subtype of PD [4,9]. Because of its sudden and unpredictable nature, FOG is an important cause of falls and a major contributor to the increased morbidity and mortality of patients with PD [3,10,11]. Gait disturbances in PD (particularly FOG), have a notable clinical impact on patients’ quality of life due to reduced mobility, loss of independence, social embarrassment, and caregiver burden [12,13].
Atypical Blepharospasm with Oromandibular Dystonia Associated with Cerebral Amyloid Angiopathy
Published in Neuro-Ophthalmology, 2022
Andrew R. Carey, Neil R. Miller
A 64-year-old man presented with a 3 week history of facial spasms for which he initially presented to a local emergency department where he underwent non-contrast MRI that was said to show no abnormalities. He was subsequently evaluated by a neurologist who prescribed lorazepam and valproic acid without relief. The patient’s past medical history was significant for mild cognitive impairment, well-controlled hypertension, dyslipidaemia, type 2 diabetes mellitus, chronic kidney disease, uncontrolled migraine with vestibular features, benign postural paroxysmal vertigo and vestibular neuritis, an L3 spinal schwannoma for which he had undergone surgery 38 years prior, and a history of head trauma and neck fracture from diving into a swimming pool 46 years earlier, requiring a C5–C7 fusion. He denied tremors, limb rigidity, trouble writing, or shuffling gait. His ocular history was significant for recurrent corneal erosions in the left eye after trauma from a hairbrush. Relevant medications include gabapentin, venlafaxine, magnesium-oxide, and aspirin 81 mg; he had previously failed nortriptyline and had some improvement with occipital nerve blocks. His family history was positive for an aunt with excessive blinking but negative for dementia, Parkinson’s disease, or intracranial haemorrhage.
Novel POLG mutation in a patient with early-onset parkinsonism, progressive external ophthalmoplegia and optic atrophy
Published in International Journal of Neuroscience, 2020
Lin Ma, Wei Mao, Erhe Xu, Yanning Cai, Chaodong Wang, Jagadish K. Chhetri, Piu Chan
The 29 year-old Chinese female patient developed right upper limb mixed rest and postural tremor at the age of 16. The tremor gradually progressed to left upper limb, lower extremities and the head. Two years later, she showed signs of parkinsonism including bradykinesia and shuffling gait. Treatment with benserazide/levodopa 25/100 mg bid and benzhexol hydrochloride 2 mg tid significantly improved tremor and bradykinesia, however, soon accompanied with severe peak-dose dyskinesia. With time the patient showed end-of-dose deterioration effect, and self-adjusted benserazide/levodopa’s dose to 12.5/50 mg q2h (about 150/600 mg per day) which helped to relieve the fluctuation. At 23 years of age, the patient developed signs of slowly progressive bilateral ptosis, and a year later, her symptoms significantly aggravated, with frequent falls because of dyskinesia and postural instability, along with development of diplopia, dysarthria and dysphagia. The patient also reported presence of mild muscles weakness and exercise intolerance conditions.