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Neurologic Diagnosis
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
Ask the patient to (you may need to demonstrate the test): Walk “heel-to-toe” to test tandem gait. Patients with a lesion of the midline cerebellar vermis may only manifest truncal ataxia and have no evidence of limb ataxia on coordination testing.Stand on one leg alone and keep balance (to be compared with your experience of age-matched controls).Romberg's test: request the patient to stand still with feet close together, first with eyes open, and then shut for 30 seconds. Notice any significant change in stability where the patient shows a tendency to actually fall (needs your support) that reflects impaired joint position sense from a spinal dorsal column deficit or severe sensory polyneuropathy or bilateral vestibular failure. Some normal subjects will show a small–moderate body sway; functional patients may show an exaggerated response.
Multiple choice questions (MCQs)
Published in Tristan Barrett, Nadeem Shaida, Ashley Shaw, Adrian K. Dixon, Radiology for Undergraduate Finals and Foundation Years, 2018
Tristan Barrett, Nadeem Shaida, Ashley Shaw, Adrian K. Dixon
Which of the following normal structures can demonstrate calcification on CT of the head? Pineal gland.Choroid plexus.Cerebellar vermis.Medulla oblongata.Habenular commissure.
Brain regions, lesions, and stroke syndromes
Published in Christos Tziotzios, Jesse Dawson, Matthew Walters, Kennedy R Lees, Stroke in Practice, 2017
Christos Tziotzios, Jesse Dawson, Matthew Walters, Kennedy R Lees
The last (but not the least important) part of the hindbrain is the cerebellum, which sits comfortably in the posterior cranial fossa. The cerebellum is formed by the two hemispheres joined by the worm-like structure known as cerebellar vermis. The cerebellum also consists of an outer layer of grey matter (cerebellar cortex) and inner white matter. Within the deeper white matter are four pairs of nuclei that interconnect with the cerebellar cortex and with certain cell body aggregates of the brainstem and thalamus. From a functional standpoint, the cerebellum is responsible for the maintenance of equilibrium and posture and skeletal muscle tone as well as coordination of movement, all at a subconscious level. A stroke in the cerebellum will cause a lack of coordination in upper and lower limbs manifesting as hypotonia or intention tremor, dysdiadochokinesis, and an ataxic, wide-based gait. When the lesion is unilateral, the deficit is likewise. When the median cerebellar vermis is involved, a vertiginous labyrinthine syndrome may result that closely mimics a peripheral vestibulopathy. A cerebellar stroke can also impair eye movement by affecting the coordinated function of extraocular musculature, thereby leading to nystagmus with the fast component pointing toward the side of the lesion. Dysarthria may ensue but is not sign specific to stroke, as it is commonly seen with bilateral cerebellar involvement, as in alcohol intoxication, hypothyroidism, and multiple sclerosis.
Neuropsychiatric systemic lupus erythematosus with cerebellar vasculitis and obstructive hydrocephalus requiring decompressive craniectomy
Published in Modern Rheumatology Case Reports, 2021
Nobuhito Naito, Hiroshi Kawano, Yuya Yamashita, Mayo Kondo, Shotaro Haji, Ryosuke Miyamoto, Yuko Toyoda, Yasuhisa Kanematsu, Yuishin Izumi, Yoshimi Bando, Yasuhiko Nishioka
However, on the second day of mPSL pulse therapy, consciousness disorder (Glasgow Coma Scale [GCS] E3V4M6) appeared suddenly, and brain computed tomography (CT) revealed cerebellar oedema with obstructive hydrocephalus caused by cerebellar oedema (Figure 3). Emergency decompressive craniectomy was performed in order to save her life. At the time of surgery, a biopsy of the cerebellar vermis was also performed. Histological examinations of the biopsy specimens showed infiltration of inflammatory cells around some blood vessels with fibrinoid necrosis, findings that were compatible with features of vasculitis (Figure 4). Given these histological findings, she was treated with additional intermittent pulse intravenous cyclophosphamide (IVCY) therapy (500 mg/m2) every 4 weeks. After surgery, her headache and consciousness disorder improved (Figure 5). The regression of the high-intensity area along the sulci of the bilateral cerebellar hemispheres was observed on MRI after the second dose of IVCY (Figure 2(C)).
Vestibulo-ocular function in patients with sporadic ataxia
Published in Hearing, Balance and Communication, 2018
Bianca Simone Zeigelboim, Kairone Fernandes Kronbauer, Anylize Wachholz Von Scheidt, Hélio Teive, Vinicius Fonseca, Jair Marques
In the current study, ENG showed greater prevalence of vestibular hypofunction (53.3%), alteration in the gaze nystagmus, multiple type (40%), rotatory test (36.7%) and optokinetic test (33.4%). Cerebellar vermis lesions cause upper limbs ataxia, head titubation, dysmetria and tremor of the eye movements, and it is that anatomical part which manifests the electrical activity along the extension of eye and neck muscles [15]. The most evidenced disorders in other studies [6,15] were the presence of positional nystagmus, irregular calibration of eye movements, spontaneous nystagmus (jerk type), gaze unidirectional/bidirectional and multiple nystagmus, optokinetic abolition, vestibular hypofunction, absence of the inhibitor effect of eye fixation, and signs of Aubry for proof of Barany.
Evaluation of antineuronal antibodies and 8-OHdG in mothers of children with autism spectrum disorder: a case-control study
Published in International Journal of Psychiatry in Clinical Practice, 2022
Şermin Bilgen Ulgar, Hamza Ayaydın, Hakim Çelik, İsmail Koyuncu, Adnan Kirmit
Almost all of the reported post-mortem examinations of individuals with autism have shown a significant reduction in the number of Purkinje cells, primarily in the posterolateral neocerebellar cortex and adjacent archicerebellar cortex of the cerebellar hemispheres (Arin et al. 1991; Whitney et al. 2008). According to some study authors, the presence of a reduced number of Purkinje cells in the brains of individuals with autism may not be common to all cases (Whitney et al. 2008). In this study, the number of Purkinje cells in the brain of three individuals of 6 patients was found to be close to those of the controls, and no correlation was found between Purkinje cell density and the severity of autism (Whitney et al. 2008). In another study, however, no abnormality was detected in Purkinje cell size or number in this region in the detailed analysis of cerebellar vermis. Therefore, as reported by cranial imaging studies, no microscopic cellular explanation for vermal hypoplasia could be provided (Courchesne et al. 1994). Evidence of late prenatal loss of Purkinje cells in the last quarter of gestation was provided by a study evaluating the number of basket cells and stellate cells that are necessary for the survival of Purkinje cells (Whitney et al. 2009). These researchers have demonstrated that there is no reduction in the number of basket and stellate cell interneurons in the cerebellar molecular layer, which means that, after Purkinje cells have been formed, they migrate to their proper sites and later die. The timing of loss of Purkinje cells appears to be prenatal. There was no detected neuron loss in the inferior olive in terms of synapses in the brains of autistic individuals with Purkinje cell loss. This tight connection is established shortly before birth. Once this connection is established, any Purkinje cell loss results in mandatory retrograde cell loss of inferior olive neurons (Whitney et al. 2008). Moreover, in the inferior olive, it has been observed that neurons were clustered around the perimeter of nuclear convolutions, a pathology pattern common to an earlier prenatal period (DeBassio et al. 1985). In our study, although we explained the relationship between anti-Ri positivity and possible cerebellum above, the anti-YO antibody levels in mothers of children with autism did not differ from the control group, operating under the assumption that exposure to prenatal anti-YO antibodies may cause Purkinje cell loss in the foetus and thus be associated with autism. In the study by Ali et al., higher levels of anti-Yo antibodies were found in the case group compared to the control group (Ali et al. 2016). This may be due to the low number of participants in our study.