MyMedR

An atypical course of a 71-year old man with right arm weakness and ataxia: Expert commentary

Mohamed Ibrahim N

Parkinsonism Relat Disord, 2022 Dec;105:157-158.

PMID: 36274018 DOI: 10.1016/j.parkreldis.2022.10.015

Matched MeSH terms: Ataxia/etiology

Fulltext A rare case of unilateral Cogan's anterior internuclear ophthalmoplegia, upgaze palsy and ataxia caused by dorsal tegmentum lesion at pontomesencephalic junction

Wai YZ, Ng QX, Lim TH, Lim LT

BMC Ophthalmol, 2021 Feb 25;21(1):105.

PMID: 33632162 DOI: 10.1186/s12886-021-01868-9

BACKGROUND: Cogan's anterior internuclear ophthalmoplegia (INO) is characterized by INO with inability to converge and commonly thought to be due to rostral midbrain lesion. A lesion outside midbrain that causes unilateral Cogan's anterior INO combined with upgaze palsy and ataxia are rarely described.

CASE PRESENTATION: A 67-year old male presented with left Cogan's anterior internuclear ophthalmoplegia (INO), left appendicular ataxia and bilateral upgaze palsy. A Magnetic Resonance Imaging (MRI) and Magnetic Resonance Angiography (MRA) brain showed a left dorsal tegmental infarct at the level of pontomesencephalic junction.

CONCLUSIONS: This case highlights the clinical importance of Cogan's anterior INO in combination with upgaze palsy and ataxia, and report possible site of lesion in patients with such constellation. Clinicians should consider looking for cerebellar signs in cases of Cogan's anterior INO, apart from just considering localizing the lesion at the midbrain.

Matched MeSH terms: Ataxia/etiology

Fulltext Typhoid fever presenting as acute cerebellar ataxia and severe thrombocytopenia

Cheong BM

Med J Malaysia, 2008 Mar;63(1):77-8.

PMID: 18935745 MyJurnal

Typhoid fever being a systemic infection can present in a multitude of ways, involving various systems. Here we describe a case of typhoid fever presenting with acute cerebellar ataxia and marked thrombocytopenia. This atypical presentation is not common in typhoid fever and can lead to misdiagnosis as well as a delay in the initiation of appropriate therapy. Prompt clinical improvement and the return of platelet counts to normal were noted after the patient was started on IV Ceftriaxone.

Matched MeSH terms: Cerebellar Ataxia/etiology*

Fulltext Syndromes of ophthalmoplegia, ataxia and areflexia - case report

Tan CT

Med J Malaysia, 1981 Sep;36(3):186-7.

PMID: 7329377

Two cases of Syndromes of Ophthalmoplegia , Ataxia and Areflexia were reported. A brief discussion on its clinical feature and differential diagnosis was made.

Matched MeSH terms: Ataxia/etiology*

Mouse model of intracerebellar haemorrhage

Tijjani Salihu A, Muthuraju S, Aziz Mohamed Yusoff A, Ahmad F, Zulkifli Mustafa M, Jaafar H, et al.

Behav Brain Res, 2016 10 01;312:374-84.

PMID: 27327104 DOI: 10.1016/j.bbr.2016.06.034

The present study aimed to investigate the behavior and neuronal morphological changes in the perihaemorrhagic tissue of the mouse intracerebellar haemorrhage experimental model. Adult male Swiss albino mice were stereotactically infused with collagenase type VII (0.4U/μl of saline) unilaterally in to the cerebellum, following anaesthesia. Motor deficits were assessed using open field and composite score for evaluating the mouse model of cerebellar ataxia at 1, 3, 7, 14 and 21 days after collagenase infusion. The animals were sacrificed at the same time interval for evaluation of perihaematomal neuronal degeneration using haematoxylin and eosin staining and Annexin V-FITC/Propidium iodide assay. At the end of the study, it was found that infusion of 0.4U collagenase produces significant locomotor and ataxic deficit in the mice especially within the first week post surgery, and that this gradually improved within three weeks. Neuronal degeneration evident by cytoplasmic shrinkage and nuclear pyknosis was observed at the perihaematomal area after one day; especially at 3 and 7 days post haemorrhage. By 21 days, both the haematoma and degenerating neurons in the perihaematomal area were phagocytosed and the remaining neuronal cells around the scar tissue appeared normal. Moreover, Annexin-V/propidium iodide-positive cells were observed at the perihaematomal area at 3 and 7 days implying that the neurons likely die via apoptosis. It was concluded that a population of potentially salvageable neurons exist in the perihaematomal area after cerebellar haemorrhage throughout a wide time window that could be amenable to treatment.

Matched MeSH terms: Cerebellar Ataxia/etiology

Forme fruste anti-GQ1b-negative Miller Fischer syndrome masquerading as posterior circulation stroke

Sim BNH, Joseph JP

J R Coll Physicians Edinb, 2019 Dec;49(4):304-306.

PMID: 31808458 DOI: 10.4997/JRCPE.2019.411

Miller Fischer syndrome (MFS) is a variant of Guillain-Barré syndrome first described in 1956 and is characterised by the clinical triad of ophthalmoplegia, ataxia and areflexia. However, since its discovery, forme fruste and overlapping syndrome have been described. A forme fruste of MFS implies an attenuated form where not all of the clinical triad are present. In this report, a case of MFS is highlighted that was mistakenly treated as posterior circulation stroke, as well as the challenges faced in reaching the correct diagnosis and hence the appropriate treatment.

Matched MeSH terms: Ataxia/etiology*

Fulltext Neonatal posterior fossa haemorrhage associated with vacuum extractor

Ghani AR, Prakash RG, Abdullah J

Med J Malaysia, 2006 Mar;61(1):100-2.

PMID: 16708744 MyJurnal

We report one case of posterior fossa intracranial haemorrhage in a full-term Malay baby boy following vacuum assisted delivery. The patient, a term baby boy was delivered by a vacuum extraction and later developed signs of increased intracranial pressure 72 hours after birth. Computed tomography (CT) of the brain showed a posterior fossa intracranial haemorrhage with acute obstructive hydrocephalus. He was initially treated with isolated ventricular shunting which later caused an upward cerebellar herniation. An immediate suboccipital craniectomy for evacuation of cerebellar haematoma was performed which resulted in a gradual recovery.

Matched MeSH terms: Cerebellar Ataxia/etiology

Development of the clinical assessment scale in autoimmune encephalitis

Lim JA, Lee ST, Moon J, Jun JS, Kim TJ, Shin YW, et al.

Ann Neurol, 2019 03;85(3):352-358.

PMID: 30675918 DOI: 10.1002/ana.25421

OBJECTIVE: There is no scale for rating the severity of autoimmune encephalitis (AE). In this study, we aimed to develop a novel scale for rating severity in patients with diverse AE syndromes and to verify the reliability and validity of the developed scale.

METHODS: The key items were generated by a panel of experts and selected according to content validity ratios. The developed scale was initially applied to 50 patients with AE (development cohort) to evaluate its acceptability, reproducibility, internal consistency, and construct validity. Then, the scale was applied to another independent cohort (validation cohort, n = 38).

RESULTS: A new scale consisting of 9 items (seizure, memory dysfunction, psychiatric symptoms, consciousness, language problems, dyskinesia/dystonia, gait instability and ataxia, brainstem dysfunction, and weakness) was developed. Each item was assigned a value of up to 3 points. The total score could therefore range from 0 to 27. We named the scale the Clinical Assessment Scale in Autoimmune Encephalitis (CASE). The new scale showed excellent interobserver (intraclass correlation coefficient [ICC] = 0.97) and intraobserver (ICC = 0.96) reliability for total scores, was highly correlated with modified Rankin scale (r = 0.86, p

Matched MeSH terms: Ataxia/etiology

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