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Assessment of the stroke patient
Published in Christos Tziotzios, Jesse Dawson, Matthew Walters, Kennedy R Lees, Stroke in Practice, 2017
Christos Tziotzios, Jesse Dawson, Matthew Walters, Kennedy R Lees
PowerTo test drift, ask ‘Shut your eyes and stretch your arms out and turn your palms upwards’. Watch for five to 10 seconds to see if either arm drifts down and pronates. A unilateral pronator drift suggests an UMN lesion on the same side. This is because of the fact that the UMN pattern of weakness causes supination of the upper limbs to be weaker than pronation. An abnormal searching movement may be seen with loss of proprioception (also known as pseudoathetosis). Upward movement may suggest cerebellar or parietal lobe deficit.Strength is tested in upper (at shoulder, elbow, wrist, and fingers) and lower limbs (at hip, knee, ankle, and tarsal joint). Muscle strength should be graded using the Medical Research Council scale (seeTable 5.9).The pattern of weakness in UMN lesions involves extensors that are weaker than flexors in arms and extensors stronger than flexors in legs.
Consequences of an incomplete differential diagnosis
Published in James W. Albers, Stanley Berent, Neurobehavioral Toxicology: Neurological and Neuropsychological Perspectives, 2005
James W. Albers, Stanley Berent
During her hospitalization, she developed involuntary movement of her fingers and toes when her eyes were closed (pseudoathetosis). She became constipated and showed erratic vital signs with severe orthostatic hypotension. She stabilized about 3 weeks after onset, leaving her with a profound sensory deficit. She had complete absence of proprioception, global decrease in touch and pin sensations, areflexia, and a cerebellar-like, ataxic gait. Repeat lumbar puncture at that time showed an elevated protein (130 mg%), but no other abnormalities.
Discussions (D)
Published in Terence R. Anthoney, Neuroanatomy and the Neurologic Exam, 2017
Although one or more additional types of movement are listed as involuntary in most of the seven texts, the treatment of any particular type is very inconsistent. For example, pseudoathetosis, which is mentioned in only five of the texts, is listed as an independent type of involuntary movement by Gilroy and Meyer (1979, p. 50), as a type of tremor by Bickerstaff (1980, p. 151–152). as an athetoid-like movement by Thornas and Dale (1981, p. 112), and is not listed as an involuntary movement at all by Walton (1975, p. 199, not p. 183–187) or by Rowland (1984, p. 162, not p. 38–41). There are at least two probable reasons for such inconsistencies. One involves levels of classification and may lead to discrepancies that are more apparent than real. In the case of hiccup, for example, Thornas and Dale list it as an independent type of involuntary movement (1981, p. 114); whereas Fahn does not mention it at all under “Involuntary Movements” (in Rowl, p. 38–41). Else where in the same text, however. Fahn classifies hiccup as “physiologic myoclonus” (p. 521), myoclonus being one of his types of involuntary' movement (p. 39). In other words. Fahn does consider hiccup to be an involuntary' movement, but he does not list it explicitly as such because he considers it to be simply one example of a more inclusive category—myoclonus.2 The lesson to be learned here is that absence of a particular type of movement from an author’s listing of involuntary movements is not sufficient evidence that she does not label it formally as an involuntary movement. It may be listed elsewhere in the same text, classified as an example of a type of movement which is included in the author’s listing of involuntary movements.
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].
A Case of Neuromuscular Electrical Stimulation for Childhood Stroke Hyperkinesis: A Brief Report
Published in Developmental Neurorehabilitation, 2020
Megan J. Metzler, Lauran Cole, Adam Kirton
The participant was a previously right-hand dominant 16-year-old female with right-sided hyperkinesis, characterized as a pseudoathetosis. Symptoms were a result of childhood hemorrhagic stroke of the left thalamus secondary to an arteriovenous malformation 3 years earlier. The participant received intensive rehabilitation initially but had not received a block of therapy for over 2 years.