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The Problems
Published in John Greene, Ian Bone, Understanding Neurology a problem-orientated approach, 2007
Ataxia on eye closure but not with open eyes is suggestive of: Cerebellar ataxia.Sensory ataxia.A positive Romberg’s test.Middle ear disease.
Gait examination
Published in Hani Ts Benamer, Essential Revision Notes in Clinical Neurology, 2017
➤ The following are the classic gait abnormalities: ➣ Hemiplegic gait – the lower limb moves in a semicircle, the toe scraping the floor with each step, and the arm is held in a flexed position close to the chest.➣ Spastic gait – a stiff, scissor gait with the legs crossing in front of each other while walking.➣ Ataxic gait – patient’s gait is wide-based ‘drunken gait’ with difficulty performing heel-to-toe test. Patients with sensory ataxia usually have severe impairment of joint position and vibration. Patients usually stamp their feet on the floor when walking. Sensory ataxia is usually due to subacute combined degeneration of the cord (vitamin B12 deficiency).➣ Parkinsonian gait – patient walks with small steps and shuffles. Patient stoops with lack of arm swing and the arms are held in flexed positions.➣ Steppage gait – patient lifts the foot high during walking to avoid scraping the toes and foot slapping. This is due to foot drop.➣ Waddling gait – There is lumbar lordosis and the patient’s legs are wide apart. The trunk moves from side to side with the pelvis dropping. This is usually due to hereditary muscular dystrophies.➣ Gait apraxia, marche à petits pas and lower-body Parkinsonism – different terms describing patients with difficulty in starting to walk with small, shuffling steps. This is an indication of diffuse cerebrovascular ischaemic disease (small-vessel disease).
Neuropsychiatric manifestations in primary Sjogren syndrome
Published in Expert Review of Clinical Immunology, 2022
Simone Appenzeller, Samuel de Oliveira Andrade, Mariana Freschi Bombini, Samara Rosa Sepresse, Fabiano Reis, Marcondes C. França
Sensory neuronopathy is the most specific and most disabling pSS-related PNS manifestation [28,34]. According to multiple reports, pSS stands as the most frequent etiology for non-paraneoplastic sensory neuronopathy [35]. Therefore, recognition of sensory neuronopathy should always prompt detailed investigation of pSS. The clinical picture is characterized by subacute (over weeks) or chronic (over months/years) appearance of multifocal sensory deficits, involving predominantly vibratory and joint-position modalities. The sensory deficit is classically multifocal and asymmetric with the absence of motor deficits [36]. There is early loss of deep tendon reflexes and emergence of sensory ataxia. Pseudoathetosis is another conspicuous feature affecting individuals who can become wheelchair bound because of worsening ataxia in the short term. Neuropathic pain can also be found in these subjects and may be extremely bothersome. A significant proportion of patients with pSS-related sensory neuronopathy develop dysautonomia, which may manifest as orthostatic hypotension, sweating abnormalities, and tonic pupils [37].
Optimal outcome measures for assessing exercise and rehabilitation approaches in chemotherapy-induced peripheral-neurotoxicity: Systematic review and consensus expert opinion
Published in Expert Review of Neurotherapeutics, 2022
Susanna B. Park, Stefano Tamburin, Angelo Schenone, Ian R. Kleckner, Roser Velasco, Paola Alberti, Grace Kanzawa-Lee, Maryam Lustberg, Susan G. Dorsey, Elisa Mantovani, Mehrnaz Hamedani, Andreas A. Argyriou, Guido Cavaletti, Ahmet Hoke
Outcome measures addressing manifestations of CIPN include neurological and neurophysiological examination and symptoms-based measures. CIPN PROMs are crucial to examine CIPN symptoms and are necessary for inclusion in core outcome measures set but may not be sufficient alone, particularly in CIPN prevention trials. CIPN PROMs are patient relevant and fulfil the increasing requirement by regulatory authorities and other bodies for clinical trials to incorporate patient-relevant endpoints [45]. Given the limitations of existing studies, it is difficult to identify the best PROM to quantify amelioration of CIPN symptoms following exercise. Further, the ideal PROM must be precise; for example, the use of neuropathic pain PROMs is appropriate solely for studies recruiting patients specifically selected to have neuropathic pain symptoms, which are typically only experienced by 25–40% of patients with CIPN [46]. Additionally, some evidence suggests that CIPN PROMs may not capture relevant changes in patient function and development of sensory ataxia in exercise trials. Therefore, the development of other measures (including PROMs focused on sensory ataxia and patient function or objective and/or semi-objective clinical assessments) should be considered.
The safety of medications used to treat peripheral neuropathic pain, part 1 (antidepressants and antiepileptics): review of double-blind, placebo-controlled, randomized clinical trials
Published in Expert Opinion on Drug Safety, 2020
Marie Selvy, Mélissa Cuménal, Nicolas Kerckhove, Christine Courteix, Jérôme Busserolles, David Balayssac
Sensitive peripheral neuropathy and its most disabling symptoms, neuropathic pain, refers to a lesion or disease of the somatosensory nervous system [1]. Peripheral neuropathy can be classified as a mixture of phenomenological, neurophysiological, pathological, and etiological parameters [2]. The most common form of peripheral neuropathy is chronic axonal length-dependent sensorimotor polyneuropathy. Neuropathic symptoms can be divided into sensory and motor symptoms. The sensory symptoms include tingling, pins/needles, numbness, tightness, burning, pain, and sensory ataxia. Motor symptoms include muscle cramps, stiffness, weakness, and wasting [3]. Peripheral neuropathy may result from various conditions, including traumatisms (e.g., amputation, surgery, nerve compression), diabetes, toxicants (e.g., neurotoxic drugs, lead, alcohol), and infectious agents (e.g., herpes zoster, leprosy) [4].