Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Saturday, August 26, 2017

Multifocal Myoclonus after Stroke and Rehabilitation-A Case Report

Does involuntary movement also include coughing and sneezing making the arm fly about?

Multifocal Myoclonus after Stroke and Rehabilitation-A Case Report

Kavitha Andiappan* and Lydia Abdul Latif
Kavitha Andiappan* and Lydia Abdul Latif
*Corresponding Author:
Kavitha Andiappan
Department of Rehabilitation Medicine
Medical Faculty, 12th floor, Menara Selatan
University Malaya Medical Centre
59100, Kuala Lumpur, Malaysia
Tel: 60123897001
E-mail: kavitha_andiappan@yahoo.com
Received Date: Jun 03, 2017 Accepted Date: Jun 23, 2017 Published Date: Jun 27, 2017
Citation: Andiappan K, Abdul Latif L (2017) Multifocal Myoclonus after Stroke and Rehabilitation - A Case Report. J Neurol Neurosci 8:3.doi: 10.21767/2171-6625.1000201
Visit for more related articles at Journal of Neurology and Neuroscience

Abstract

Movement disorders are a rare recognized complication of stroke. Different types of hyperkinetic and hypokinetic movement disorders have been reported and can be seen after ischemic and haemorrhagic strokes. Failure to address these involuntary movements poses a challenge for post-stroke intensive multidisciplinary rehabilitation. We describe a patient presenting with multifocal myoclonus after an Anterior Cerebral Artery (ACA) territory infarct whose symptoms were brought under control with clonazepam. Additionally, we discussed on our experience and the challenges faced in the diagnostic process, management, and rehabilitation of this patient.

Keywords

Myoclonus after stroke; Rehabilitation

Introduction

Movement disorders are a recognised complication of stroke. Reported frequency of involuntary movements following stroke ranges between 1-4% [1-3]. Although rare, many different varieties of abnormal movement can be found after a stroke either acutely or as a delayed sequel. They can be hyperkinetic (most commonly hemichorea–hemiballismus) or hypokinetic (most commonly vascular parkinsonism). Most are caused by lesions in the basal ganglia or thalamus but can occur with strokes at many different locations in the motor circuit [3]. Among these, myoclonus is one of the rarest form of movement disorder in patients with stroke [1]. Myoclonus is described as sudden, brief, shock like, involuntary movements caused by muscular contractions [4]. Myoclonus after a stroke has been so far reported to be focal or segmental with posterior circulation strokes, particularly midbrain, pontine, and thalamic strokes [1,2]. However, no multifocal myoclonus following a stroke has been reported prior to this [1].

Case Report

A 59-year-old gentleman of no known medical illness initially presented to the hospital with one day history of sudden onset of left-sided limb weakness. The blood pressure upon presentation was 190/107 mmHg. 2 days prior to the presentation, he had what he described as a sudden twitching of the left lower limb lasting for about 5 minutes and resolved spontaneously. He was conscious and aware of the involuntary movement but was unable to control it. Upon presentation to the hospital, it was noted that he had left upper motor neuron facial nerve palsy with left-sided hemiparesis with a general muscle power of 4/5 according to the Medical Research Council (MRC) grading system on the left side. Glasgow Coma Scale (GCS) level was full at all times. Computer Tomography (CT) scan of the brain showed less well defined hypodensity at the right centrum semiovale.
On the 2nd day, the left-sided weakness progressively worsened till it was dense flaccid left hemiparesis. There were also increasing occurrences of jerky movements of the left upper limb, abdomen, and lower limb with each episode lasting 2 to 3 minutes each time without any loss of consciousness. Repeated CT scan of the brain showed early subacute right ACA territory infarct (Figure 1). Electroencephalogram (EEG) did not reveal any epileptic form discharges throughout the recording despite the fact that the patient had 1 episode of involuntary movement of the abdomen during the EEG procedure. He was diagnosed to have right ACA infarct with epilepsia partialis continua (EPC). Antiepileptic agent, oral sodium valproate 400 mg thrice a day, was initiated. The involuntary movements became less frequent with medication.

No comments:

Post a Comment