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Haematology and oncology
Published in Jagdish M. Gupta, John Beveridge, MCQs in Paediatrics, 2020
Jagdish M. Gupta, John Beveridge
9.36. Clinical features of posterior midline cerebellar tumour includevisual field defects.truncal ataxia.stiff neck.dystonia.papilledema.
Disorders of Sensation, Motion, and Body Schema
Published in Rolland S. Parker, Concussive Brain Trauma, 2016
The vermis controls structures that are axial or that are bilaterally innervated (i.e., station and gait)—walking and coordination of the head and trunk. A patient with a mild vermian lesion has gait ataxia, where the base is widened, tandem gait is very difficult, and there may be decompensation on turning. With truncal ataxia, there is swaying and unsteadiness when standing and an inability to maintain upright posture. There is little or no abnormality of the extremities, although all coordinated movements may be poorly performed. Patients are more variable on motor tasks that require precise temporal representation. A difference between sensory ataxia (loss of proprioception) and cerebellar ataxia is that while in sensory ataxia, performance is not normal with eyes open, it worsens markedly with eyes closed. Tremor is due to voluntary visually guided corrections to deviations from the intended track. With cerebellar ataxia, it makes little difference whether or not there is vision to guide movement (Campbell, 2005, pp. 522–524). Patients with varied cerebellar degeneration have difficulty in the expression and timing of a conditioned eyeblink response (Topka et al., 1993).
History and physical examination
Published in Alistair Burns, Michael A Horan, John E Clague, Gillian McLean, Geriatric Medicine for Old-Age Psychiatrists, 2005
Alistair Burns, Michael A Horan, John E Clague, Gillian McLean
Next move to the arms, which need to be exposed suf�iciently for you to measure the blood pressure: do this yourself and do not rely on the chart. Arms greater than 27cm circumference ind�cate the need for a cuff larger than the standard one to avoid overestimating the true blood pressure. If there is a history of any 'funny turns' or blackouts, check the blood pressure in both arms (subclavian steal syndrome). In the presence of atrial fibrilla- tion, blood pressure measurements will be inaccurate unless a special tech- nique is used (not described here). Check the pulse rate and rhythm. Look for evidence of joint disease and tophi. Bruising at this location is common, and comes about after minor trauma to thin skin with fragile blood vessels (senile purpura). Feel around the elbow for rheumatoid nodules. Check the upper limb tend�n reflexes. Detailed sensory testing is not necessary, but check for gross sensory loss or sensory inattention. Check for upper-limb ataxia with the fmger-nose test. Truncal ataxia will already have been assessed by watching the patient's ability to sit upright, unsupported, on a chair. A useful screen for sensory and motor impairments as well as joint malfunction is to ask the patient to try to scratch his/her back between the shoulder blades, using each arm in turn, and to manip�late small objects with the hands (e.g. undo and fasten a button). Test muscle strength at the shoulder (abduction) and observe the arm for fasciculations. Observe for abnormal movements at rest, while sustaining a fixed posture and during movement.
Miller Fisher syndrome and Guillain-Barré syndrome: dual intervention rehabilitation of a complex patient case
Published in Physiotherapy Theory and Practice, 2022
Jill E. Mayer, Christine A. McNamara, John Mayer
The impact of aquatic therapy in reducing or controlling for truncal ataxia has not been studied. However, given the properties of water, particularly hydrostatic pressure and viscosity, this environment may be beneficial in improving functional outcomes in the presence of ataxia (Becker, 2009). Outcome measures that measure ataxia and consider its effects on function and balance could have been included. The Scale for the Assessment and Rating of Ataxia is a valid and reliable measure of ataxia (Schmitz-Hübsch et al, 2006). In addition, the International Cooperative Ataxia Rating Scale quantifies the impact of ataxia in functional activities such as walking and standing (Schmitz‐Hübsch et al, 2006; Trouillas et al, 1997). Utilizing these measures would have likely been more appropriate than the BBS to measure potential changes in postural control. More clinical trials are needed to determine if the combination of interventions can demonstrate similar or even greater effectiveness in patients with complex symptom presentations.
Ataxia-telangiectasia: epidemiology, pathogenesis, clinical phenotype, diagnosis, prognosis and management
Published in Expert Review of Clinical Immunology, 2020
Parisa Amirifar, Mohammad Reza Ranjouri, Martin Lavin, Hassan Abolhassani, Reza Yazdani, Asghar Aghamohammadi
In A-T patients, progressive gait and truncal ataxia are the main aspects of clinical manifestations. The progressive spinocerebellar neurodegeneration usually manifests between the ages of 1–4 years. At the beginning of their second decade, the movement problems typically cause a child to use a wheelchair [52]. Patients with A-T present with cerebellar dysfunction, including ataxia, hypotonic muscles, dyssynergia, truncal swaying, and balance difficulties [53]. They may develop increasing difficulty with abnormal involuntary movements, including dystonia, dysphagia, chorea and athetosis. Overall, a severe form of chorea, choreoathetosis, and dystonia are found in almost all patients with A-T [54,55]. Myoclonic jerking and various rhythmic tremors are observed in a quarter of patients.
Novel compound heterozygous mutations causing Kufs disease type B
Published in International Journal of Neuroscience, 2018
Cui Wang, Hongliang Xu, Yun Yuan, Yajun Lian, Nanchang Xie, Liang Ming
The proband of this family was a 32-year-old female teacher (Figure 1). At 30 years old, the patient presented with memory deficits and behavioural disturbances (hypomnesia, dyscalculia and nonsensical language). The symptoms became progressively worse, and motor features appeared, including tremor, bradykinesia and extrapyramidal type rigidity. She had completed her college studies and had no relevant past medical history. Neurological examination on admission revealed poor intelligence and memory, and disorientation, tremor, and cogwheel rigidity of the bilateral upper limbs and truncal ataxia. The remaining neurological examinations were normal. A detailed review of her family history was negative for neurological and psychiatric diseases. There was no consanguinity between her parents.