Recurrent Episodes Of Dizziness Research Articles

Benign paroxysmal vertigo of childhood: A case report

Benign Paroxysmal Vertigo of Childhood (BPVC) is a disorder characterized by recurrent episodes of dizziness which are often sudden, occurring in the first decade of life, last a few seconds to one minute, recover completely after the episode and often would re-occur several times a month for several years. The present case study was to highlight the clinical features of BPVC in a 3 year old female child. Audiologists must be well aware of the typical features and clinical perspectives of BPVC.

239 New de novo mutation in CACNA1a gene leading to episodic ataxia type 2

Introduction andAimEpisodic ataxia (EA) is a group of inherited ion channel disorders affecting the cer- ebellum characterised by sporadic episodes of ataxia (Riant et al, 2011; Tomlinson et al, 2013). At least 7 different types have been identified, type 2 being the most common. We describe a patient present- ing with recurrent episodes of dizziness and gait disturbance with a novel mutation in CACNA1a gene (c.586del) leading to episodic ataxia type 2.Clinical presentationA 65-year old male presented with recurrent episodes of dizziness and gait distur- bance, which had been present since childhood but increased in severity over last 2 years and leading to hospitalisation. He also reported mild cognitive impairment. Examination showed bilateral horizontal jerky nyastagmus with an otherwise normal neurological examination.InvestigationsNeuroimaging studies showed mild small vessel disease. Genetic sequencing revealed a heterogenicity for the c.586del likely pathogenic frameshift mutation in exon 4 of the CACNA1A gene, resulting in targeting of the mRNA for nonsense- mediated decay or the production of a truncated protein leading to the diagnosis of autosomal dominant episodic ataxic type 2 in this patient.SummaryWe report a new de novo mutation in CACNA1a gene leading to episodic ataxia type 2. The patient was given acetazolamide (250mg/day) which improved his symptoms. Episodic ataxia should be considered in patients presenting with a history of intermittent dizziness.kitwu@doctors.org.uk

Investigating dysautonomia of Bradbury Eggleston syndrome: A case report

This is a report of 65 years old man with recurrent episodes of dizziness while standing from supine position and history of constipation and nocturia since last 6 months. Patient disclosed no significant past history other than treated pulmonary tuberculosis 5 years back. The general mental state and vital parameters were within normal limits. Autonomic function tests and heart rate variability analysis measured autonomic reactivity and tone respectively. The tests revealed that autonomic dysfunction include severe sympathetic and mild parasympathetic involvement. After exclusion of other possible causes of orthostatic hypertension, diagnosis of pure autonomic failure also known as Bradbury Eggleston syndrome was established. Treatment with fludrocortisones and non-pharmacological interventions improved orthostatic tolerance.

Unmasking of myopotential oversensing by an integrated bipolar defibrillator lead following AV node ablation

A 73-year-old man with nonischemic cardiomyopathy underwent catheter ablation of ventricular tachycardia that had resulted in frequent shocks from his implanted cardiac resynchronization therapy defibrillator (CRT-D). Coexisting atrial fibrillation required AV node ablation which rendered the patient pacemaker dependent. During follow-up, recurrent episodes of dizziness occurred caused by inhibition of pacing due to oversensing of pectoral muscle myopotentials. Surgical revision was performed and the intraoperative examination revealed an intact integrated bipolar defibrillator lead with appropriate connections to the CRT-D header. The placement of an additional pace/sense lead completely resolved the patient's symptoms and no further myopotential oversensing was recorded.

Emery–Dreifuss muscular dystrophy with cardiac manifestations

An asymptomatic 40-year-old man attended clinic for cardiology assessment before cataract surgery. He had been diagnosed 9 years earlier with a ‘non specified limb-girdle muscular dystrophy’ following investigation for lower limb muscle weakness. Earlier electrocardiograms (ECGs) showed a bradycardic, junctional escape rhythm of 30–40 beats per minute (BPM). He had previously refused pacemaker insertion. He denied any syncope, shortness of breath or palpitations. He had muscle wasting to his upper arms and calves plus mild elbow contractures. He was normotensive, resting regular heart rate = 42 BPM and cardiorespiratory examination was unremarkable. His ECG showed atrial fibrillation, with a slow junctional escape rhythm of approximately 40 BPM and normal QRS width (Figure 1). Blood tests showed no haematological, electrolyte or thyroid dysfunction and no impaired glucose tolerance. Echocardiography showed good left ventricular function and 24-hour ECG Holter monitoring showed 8 pauses (longest 2.13s), with a heart rate varying between 29 and 79 BPM. He was commenced on clopidogrel to prevent thromboembolic complications and then he agreed for a VVIR system to be implanted to avoid bradyarrhythmic death. No complications ensued and he remains well at present. The patient also had two brothers, one died suddenly and the cause of death was not clearly determined. His elder brother was 52 years old and was diagnosed with a non-specific muscular dystrophy also associated with a junctional rhythm. He had a VVIR permanent pacemaker inserted in April 2003 following recurrent episodes of dizziness. An hereditary skeletal myopathy in association with pathognomic cardiac abnormalities suggested a diagnosis of Emery–Dreifuss muscular dystrophy (EDMD). Prognostically and therapeutically a definitive genetic diagnosis was required. Genetic testing confirmed that both siblings had inherited the X-linked form of EDMD involving a single base change of the emerin gene.

Rituximab induces remission of cerebral ischemia caused by thrombotic thrombocytopenic purpura

This report describes the experience of a case of atypical thrombotic thrombocytopenic purpura (TTP) whose diagnosis was based on severe deficiency of the von Willebrand factor (vWF) cleaving metalloprotease ADAMTS13. The level of ADAMTS13 activity, the titer of the inhibitors of this protease and the size distribution of vWF multimers in plasma samples were analysed in a patient with recurrent episodes of dizziness and blurred vision. In the absence of thrombocytopenia or microangiopathic hemolysis, diagnosis of TTP was established by demonstration of very low ADAMTS13 activity levels and the presence of inhibitors of this protease. After rituximab therapy decreased the inhibitor titer and increased the ADAMTS13 level, the patient has had no relapse of ischemic symptoms in the following 16 months. Acute neurological deficits may occur in TTP without concurrent thrombocytopenia or microangiopathic hemolysis. The role of rituximab for patients with TTP deserves further exploration.

Extended antidepressant maintenance and discontinuation syndromes

Unipolar and bipolar depression are episodic, recurrent illnesses for the majority of patients. Because each episode engenders considerable costs for patients, families, and society, prevention of recurrences has high priority. Numerous studies demonstrate that maintenance antidepressants or mood stabilizing medications are efficacious in preventing recurrences. A review of maintenance studies supports the view that all antidepressants perform significantly better than placebo in preventing recurrences of depression--with the stipulation that full antidepressant doses be employed. Earliest studies, conducted two decades ago, evaluated tricyclics (TCAs), heterocyclics, and lithium, while recent studies have focused on selective serotonin reuptake inhibitors (SSRIs). Compliance is essential. Strategies for enhancing compliance include selection of medications with reported safety and few side effects, education of patients and families, referral to patient advocacy groups, and use of new technological compliance aids. Preliminary data suggest that SSRIs are better tolerated than TCAs; fewer patients discontinue these agents due to side effects. Selection criteria for maintenance treatment have not been well determined, but three or more prior episodes is recognized as a relatively strong indicator. Other clinical or genetic criteria have also been suggested. For various reasons, patients may discontinue medications, and when this happens withdrawal phenomena may occur. Withdrawal effects are well documented for all antidepressants and can be profound with TCAs. After stopping some SSRIs, a few withdrawal symptoms may have similarities with those following discontinuation of TCAs, but unique "CNS-like" effects are frequently described, including brief recurrent episodes of dizziness, lightheadedness, vertigo, electric shock-like sensations, and gait instability. These appear to be half-life dependent, with agents with shorter half-lives having more discontinuation symptoms. If antidepressant medications must be discontinued, a gradual taper is preferable, perhaps extending three to six months or longer to prevent discontinuation effects, enable adaptation at the receptor level and allow earlier recognition and treatment of recurrent depressive symptoms.

Extended antidepressant maintenance and discontinuation syndromes.

Unipolar and bipolar depression are episodic, recurrent illnesses for the majority of patients. Because each episode engenders considerable costs for patients, families, and society, prevention of recurrences has high priority. Numerous studies demonstrate that maintenance antidepressants or mood stabilizing medications are efficacious in preventing recurrences. A review of maintenance studies supports the view that all antidepressants perform significantly better than placebo in preventing recurrences of depression--with the stipulation that full antidepressant doses be employed. Earliest studies, conducted two decades ago, evaluated tricyclics (TCAs), heterocyclics, and lithium, while recent studies have focused on selective serotonin reuptake inhibitors (SSRIs). Compliance is essential. Strategies for enhancing compliance include selection of medications with reported safety and few side effects, education of patients and families, referral to patient advocacy groups, and use of new technological compliance aids. Preliminary data suggest that SSRIs are better tolerated than TCAs; fewer patients discontinue these agents due to side effects. Selection criteria for maintenance treatment have not been well determined, but three or more prior episodes is recognized as a relatively strong indicator. Other clinical or genetic criteria have also been suggested. For various reasons, patients may discontinue medications, and when this happens withdrawal phenomena may occur. Withdrawal effects are well documented for all antidepressants and can be profound with TCAs. After stopping some SSRIs, a few withdrawal symptoms may have similarities with those following discontinuation of TCAs, but unique "CNS-like" effects are frequently described, including brief recurrent episodes of dizziness, lightheadedness, vertigo, electric shock-like sensations, and gait instability. These appear to be half-life dependent, with agents with shorter half-lives having more discontinuation symptoms. If antidepressant medications must be discontinued, a gradual taper is preferable, perhaps extending three to six months or longer to prevent discontinuation effects, enable adaptation at the receptor level and allow earlier recognition and treatment of recurrent depressive symptoms.

Value of non-invasive continuous blood pressure monitoring in the detection of carotid sinus hypersensitivity

A patient with recurrent episodes of dizziness and blackouts is described. Detailed cardiac and neurological investigations were normal. Autonomic assessment excluded postural hypotension and confirmed normal sympathetic vasoconstrictor function. Cardiac parasympathetic function in response to deep breathing, hyperventilation and ocular pressure was normal. Left carotid sinus massage only reproducibly lowered blood pressure with minimal change in heart rate. This occurred mainly during head-up tilt. The fall in blood pressure was not affected by the muscarinic blocker atropine, or the peptide release inhibitor, octreotide. A diagnosis of left carotid sinus hypersensitivity of the vasodepressor variety was made. Left carotid sinus denervation was performed. This successfully prevented further episodes of dizziness and blackouts. The ability to measure beat-to-beat blood pressure non-invasively was of particular importance in diagnosis, and in the assessment of management options in this patient.