scholarly journals Creutzfeldt–Jakob disease-like syndrome induced by gabapentin toxicity

2010 ◽  
Vol 1 (1) ◽  
pp. 3 ◽  
Author(s):  
Vicky Chau ◽  
Sadhana Prasad ◽  
Dwight Stewart ◽  
George Heckman
Keyword(s):  
Cognitive Impairment ◽  
Drug Toxicity ◽  
Clinical Manifestations ◽  
Drug Induced ◽  
Eeg Abnormalities ◽  
Negative Myoclonus ◽  
History Of ◽  
Jakob Disease ◽  
Neurological Effects ◽  
Gait Abnormalities

Patients with Creutzfeldt–Jakob disease (CJD) may exhibit characteristic abnormalities on the electroencephalogram (EEG). However, these abnormalities have been associated with a number of cases of drug toxicity. We report a case of CJD-like syndrome associated with gabapentin. A 78-year-old man was hospitalized for recurrent falls. Three months prior to admission, gabapentin was prescribed to treat symptoms of trigeminal neuralgia. The patient subsequently presented with a two-month history of worsening gait abnormalities, negative myoclonus, and cognitive impairment. The EEG showed diffuse background slowing with larger amplitude delta discharges, which at times appeared triphasic, raising the possibility of CJD. The gait abnormalities and myoclonus resolved and the EEG normalized after the gabapentin was discontinued. Several cases of drug-induced CJD-like syndrome have been reported, mainly presenting with cognitive impairment, myoclonus, Parkinsonism, and EEG abnormalities. This patient may have been predisposed to adverse neurological effects from gabapentin owing to age, concurrent renal insufficiency, and cardiac disease. We concluded that it is imperative to include drug toxicity in the differential diagnosis of patients presenting with clinical manifestations and EEG findings suggestive of CJD, particularly in the setting of advanced age and comorbidities.

scholarly journals COVID-19 and Cognitive Impairment: A Cross-Sectional Clinic Based Study

2021 ◽  
Author(s):  
Amira Siddig ◽  
Khabab Abbasher Hussien Mohamed Ahmed ◽  
Ahmed Abdelrahman ◽  
AlHussien Abbasher ◽  
Abubaker Alsedig Abbasher ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Cognitive Functions ◽  
Age Distribution ◽  
Clinical Manifestations ◽  
Cross Sectional Study ◽  
Cross Sectional ◽  
Senior Consultant ◽  
Presenting Symptoms ◽  
Phonemic Fluency ◽  
History Of

Abstract Background: Patients with dementia are more prone to acquire COVID-19 infection. Patients with COVID-19 showed a tendency to develop cognitive impairment. Objectives: We aimed to study the clinical manifestations of COVID-19 infection among adult Sudanese demented patients and the prevalence of cognitive impairment among adult Sudanese non demented patients. Methodology: This is a descriptive cross-sectional study which took place in Sudan, Khartoum state in the period (September-December 2021) in a private neurology/psychiatry clinic. 135 adult Sudanese patients were included in this study and were divided into two groups. The first group consists of 100 patients with a known history of dementia that got infected recently with COVID-19, while the second group consists of 35 patients who developed some sort of cognitive impairment after recovering from COVID-19 infection. Regarding the second group, cognitive functions were assessed by senior consultant neurologist and senior consultant psychiatrist using a well validated neuropsychological measure. Results: Out of 100 patients in the first group, females were 60 and males were 40. Age distribution is between 63 -98. The common presenting symptoms of COVID-19 among this group were: Cough and fever (90 patients), diarrhea and vomiting (5 patients), breathlessness (4 patients), coughing of blood (5 patients), convulsions (1 patient), paraplegia (1 patient) and hemiplegia (1 patient). Regarding the second group, Age distribution varied from 30 to 80 years. Cognitive functions impairment was noticed as follows: Memory recall (22%), memory recognition (23%), memory encoding (24%), processing speed (16%), executive functioning (19%), phonemic fluency (17%) and category fluency (17%). Conclusion: Patients with dementia are more susceptible to develop COVID-19 infection. Patients with COVID-19 Infection are at risk of developing some sort of cognitive impairment after recovery.

Developments in the Immunotherapy of Glomerular Disease

2002 ◽  
Vol 15 (6) ◽  
pp. 472-489
Author(s):  
Patrick H. Nachman ◽  
Jeffrey Martin
Keyword(s):  
Alkylating Agents ◽  
Clinical Manifestations ◽  
Calcineurin Inhibitors ◽  
Immunosuppressive Drugs ◽  
Glomerular Disease ◽  
Drug Induced ◽  
Glomerular Diseases ◽  
Care Givers ◽  
Clinical Syndromes ◽  
History Of

Glomerular diseases span a broad spectrum of clinical syndromes, with varied clinical manifestations, underlying etiologies, and pathogenic mechanisms. They can be secondary to underlying infectious, toxic, environmental, or drug exposures, or present as “primary entities.” In the latter case, most glomerular diseases are thought to be due to autoimmune dysregulation, and their treatment is primarily immunosuppressive. The armamentarium for immunomodulation includes corticosteroids, alkylating agents, anti-metabolites, calcineurin inhibitors, and new biological agents designed to block specific inflammatory pathways. The choice of therapy for an individual patient must be based on the specific character of the glomerular disease and its acuity and severity, as well as the patient’s comorbidities, history of prior exposure to immunosuppressive drugs, and risk factors for developing complications of the disease or its treatment. The complexities of such therapy can best be addressed by an experienced team of care givers in which the clinical pharmacist can help minimize, if not eliminate, potential sources of drug induced toxicities and adverse effects. This article will describe the major agents and modalities used in the management of the most common glomerular diseases.

scholarly journals Insidious-onset, non-wheezing carteolol-induced asthma in an atopic patient without asthma history

2019 ◽  
Vol 12 (4) ◽  
pp. e229343 ◽  
Author(s):  
Jo-Hsuan Wu ◽  
Jih-Shuin Jerng ◽  
Chien-Chia Su
Keyword(s):  
Pulmonary Function ◽  
Pulmonary Function Test ◽  
Clinical Manifestations ◽  
Eye Drops ◽  
Drug Induced ◽  
Previous Diagnosis ◽  
Insidious Onset ◽  
Function Test ◽  
History Of ◽  
Associated Risk Factors

Carteolol, a non-selective beta-antagonist with a potential risk of severe bronchial constriction in patients with asthma, is one of the most commonly prescribed medication for managing ocular pressure in glaucoma. We present a case of a 24-year-old woman with a history of atopy but no known asthma who presented an insidious onset of clinical manifestations compatible with drug-induced asthma after the initiation of carteolol for ocular hypertension control. The patient developed progressive chest tightness and dyspnoea for 2 months before the pulmonary function test revealed a positive bronchoprovocation response. She reported significant improvement of respiratory symptoms within 2 weeks after the discontinuation of carteolol, and a negative provocation response was later confirmed by repeat pulmonary function test. In conclusion, eye drops with non-selective beta-antagonising effect can induce asthmatic symptoms in patients without a previous diagnosis of asthma and should be administered with caution in patients with associated risk factors.

062 Cadasil presenting with focal and generalised epilepsy due to a novel NOTCH3 mutation

2018 ◽  
Vol 89 (6) ◽  
pp. A25.3-A26 ◽  
Author(s):  
Benson S Chen ◽  
James C Cleland ◽  
Richard I King ◽  
Neil E Anderson
Keyword(s):  
Cognitive Impairment ◽  
Genetic Testing ◽  
Cognitive Decline ◽  
Small Vessel Disease ◽  
Family Members ◽  
Clinical Manifestations ◽  
Prior History ◽  
Notch3 Mutation ◽  
History Of ◽  
Strong Segregation

IntroductionCerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is a hereditary small vessel disease caused by mutations of the NOTCH3 gene. Clinical manifestations include migraine, recurrent ischaemic strokes, and cognitive decline. Seizures are an uncommon early symptom and usually occur after the onset of stroke. We report a CADASIL family with epilepsy as an early clinical symptom due to a novel NOTCH3 mutation.MethodsThe clinical histories of three family members from two generations are reported, alongside para-clinical details including results of magnetic resonance imaging (MRI), electroencephalogram (EEG), and genetic testing.ResultsThe proband developed focal and generalised seizures at age 51. She had a preceding history of cognitive impairment and migraines. The proband’s son developed focal seizures at age 25 involving his left arm and then generalised seizures. He experienced intermittent headaches, without history of stroke or cognitive impairment. His sister (the proband’s daughter) had epilepsy from age 12, characterised by blank spells and generalised seizures. Cognitive decline was noted from age 38, without history of stroke. There was no family history of epilepsy in those without CADASIL. MRI in all three family members showed multifocal T2 FLAIR hyperintensities within the supratentorial white matter, particularly the temporal lobes. EEG was abnormal only in the proband’s son, with paroxysmal bursts of poorly organised 3–4 Hz spike-wave activity. Genetic testing in all three family members found a novel NOTCH3 mutation, c.1337G>A p.(Cys446Tyr).ConclusionWe have identified a novel NOTCH3 mutation in a kindred with epilepsy as an early manifestation of CADASIL without prior history of strokes. The association with epilepsy is unlikely to be coincidental given the strong segregation of epilepsy and CADASIL in this kindred and the clear focal seizure semiology noted in all family members. Whether this mutation represents a distinct new phenotype requires further investigation.

047 Creutzfeld-jakob disease with prolonged disease course in two younger patients

2018 ◽  
Vol 89 (6) ◽  
pp. A20.1-A20
Author(s):  
Roshan Dhanapalaratnam ◽  
Roy Beran ◽  
Michael Buckland ◽  
Cecilia Cappelen-Smith
Keyword(s):  
Cognitive Impairment ◽  
Symptom Onset ◽  
Prnp Gene ◽  
Disease Course ◽  
Post Mortem ◽  
Status Spongiosus ◽  
Younger Patients ◽  
Mri Brain ◽  
History Of ◽  
Jakob Disease

IntroductionSporadic Creuzfeldt-Jakob disease (sCJD) is a rare disease caused by prion proteins and usually presents in the 7th decade of life. sCJD classically presents with a rapidly progressive dementing illness, associated myoclonus and a median time to death of 6 months. Less commonly younger patients are described with a neuropsychiatric presentation and a prolonged disease course. We report two young sCJD patients with neuropsychiatric presentations and slow disease progression admitted to Liverpool Hospital, Sydney (2016–2017).Case 1 A 48 year old Chinese man presented with a 12 month history of depressive symptoms and insomnia. Over the next 5 months, he developed progressive cognitive impairment, disinhibited behaviour, aggression, paranoia and ataxia of gait. Serial EEG and MRI brain scans, cerebrospinal fluid (CSF) testing for 14–3–3 protein and PRNP gene testing were negative or non-contributory. He progressively became mute, bedbound and died at 24 months from symptom onset. Diagnosis was only confirmed with a limited brain autopsy at post-mortem that revealed severe microvacuolar change, gliosis, neuronal loss and status spongiosus. Anti-prion antibody 12 F10 staining showed a diffuse fine synaptic pattern in the frontal cortex and striatum consistent with sCJD.Case 2 A 42 year old Afghani man presented with a 36 month history of emotional lability and progressive social withdrawal followed by auditory and visual hallucinations, cognitive impairment and gait ataxia. Screening for vasculitis, infective (including HIV/syphilis) and autoimmune encephalopathies were negative. EEG demonstrated non-specific slowing, without characteristic periodic sharp-wave complexes. MRI brain was initially normal but progress imaging showed bilateral cortical ribboning, caudate nucleus T2-hyperintensity and associated diffusion restriction consistent with sCJD. CSF 14–3–3 protein analysis was positive. The patient died 38 months from symptom onset. Post-mortem examination was not performed.ConclusionsCJD in younger patients may present as a slowly progressive neuropsychiatric disorder and ante-mortem investigations may remain negative. Post-mortem remains the gold standard for CJD diagnosis.

scholarly journals Severe, Persistent and Fatal Delirium in Psychogeriatric Patients Admitted to a Psychiatric Hospital

2015 ◽  
Vol 5 (2) ◽  
pp. 253-264 ◽  
Author(s):  
Ingrid S. Jans ◽  
Letty Oudewortel ◽  
Paulien M. Brandt ◽  
Willem A. van Gool
Keyword(s):  
Cognitive Impairment ◽  
Medical Records ◽  
Dementia With Lewy Bodies ◽  
Fatal Outcome ◽  
Case Series ◽  
Lewy Bodies ◽  
Inclusion Criteria ◽  
Disease Trajectory ◽  
History Of ◽  
Jakob Disease

Background/Aims: Although delirium is generally regarded as a transient syndrome, persistence of delirium in patients with cognitive impairment - even with fatal outcome - has been reported as well. This study aims to describe the clinical features and neuropathological correlates of this type of delirium. Methods: Inclusion criteria for this case series were: (1) severe persistent delirium until death, (2) history of cognitive decline and (3) consent for brain autopsy. Medical records were examined in combination with collected clinical data and neuropathological findings. Result: In 15 patients, all living at home before admission, episodes with delirium lasted for 4.2 months on average. No distinct medical causes of persistent delirium could be identified. Pathological diagnoses included Alzheimer's disease and dementia with Lewy bodies as well as single cases of Creutzfeldt-Jakob disease and progressive supranuclear palsy. Conclusion: Severe, persistent and fatal delirium in patients with cognitive impairment can occur relatively early in the disease trajectory and is associated with diverse neuropathologies.

scholarly journals The Association between EEG Abnormality and Behavioral Disorder: Developmental Delay in Phenylketonuria

2012 ◽  
Vol 2012 ◽  
pp. 1-4 ◽  
Author(s):  
Parvaneh Karimzadeh ◽  
Mohammad Reza Alaee ◽  
Hadi Zarafshan
Keyword(s):  
Developmental Delay ◽  
Behavioral Disorders ◽  
Clinical Manifestations ◽  
Behavioral Disorder ◽  
Screening Tests ◽  
Eeg Abnormalities ◽  
Significant Difference ◽  
Epileptic Discharges ◽  
History Of

Background. Brain defect leading to developmental delay is one of the clinical manifestations of phenylketonuria. The aim of this study was to evaluate the association between EEG abnormality and developmental delay/behavioral disorders in phenylketonuria. Patients and Methods. 105 phenylketonuria patients, who were diagnosed through newborn screening tests or during follow-up evaluation, were enrolled. Patients who were seizure-free for at least six months before the study were included. The developmental score were evaluated by the ASQ questionnaire (age-stage questionnaire) and the test of child symptom inventory-4 (CSI-4), respectively. Results. 55 patients had a history of seizure more than 6 months before the study. Seventy had abnormal EEG (cases) and 35 had normal EEG (controls). There was no significant difference between mean phenylalanine levels in the abnormal and normal EEG groups at the time of diagnosis, after six months and at our evaluation. Distribution of DQ level in the abnormal and normal EEG groups revealed a significant difference. An abnormal EEG was associated with a higher percentage of low DQ levels. Conclusion. Paroxysmal epileptic discharges in PKU patients are important. Treatment of these EEG abnormalities may affect developmental scores or may lead to correction of some behavioral disorders in patients.

Drugs associated with drug-induced hyponatremia. Focus on antihypertensive drugs and proton pump inhibitors

2021 ◽  
Vol 1 (29) ◽  
pp. 40-46
Author(s):  
A. I. Listratov ◽  
E. V. Aleshckovich ◽  
O. D. Ostroumova
Keyword(s):  
Risk Factors ◽  
Proton Pump Inhibitors ◽  
Proton Pump ◽  
Sodium Level ◽  
Antihypertensive Drugs ◽  
Clinical Manifestations ◽  
Electrolyte Disorders ◽  
Drug Induced ◽  
Effective Prevention ◽  
History Of

Hyponatremia (HN) is one of the leading water-electrolyte disorders in daily medical practice. A decrease in sodium level is dangerous with the development of various complications. Therefore, for effective prevention of HN and its complications, special attention should be paid to modifiable risk factors. One of the important causes leading to HN is drugs. Most often, HN develops during therapy with thiazide and thiazidelike diuretics. Risk factors for its development are history of thiazide-induced HN, advanced age, female sex, low body weight, and hypokalemia. The problem of thiazide-induced HN requires further study of the pathogenetic mechanisms and determination of the genetic factors underlying it. It is also necessary to remember about the possibility of HN development against the background of such drugs widely used in therapeutic practice as blockers of the renin-angiotensin-aldosterone system and proton pump inhibitors. In patients receiving therapy with the listed drugs, it is necessary to pay attention to the possible clinical manifestations of HN and to determine the sodium level in dynamics, which will effectively prevent the development of this disorder.

scholarly journals Albendazole-induced liver injury: a case report

2013 ◽  
pp. 118-120 ◽  
Author(s):  
David Ríos ◽  
Juan Carlos Restrepo
Keyword(s):  
Case Report ◽  
Liver Injury ◽  
Drug Toxicity ◽  
Laboratory Tests ◽  
Clinical Record ◽  
Drug Induced ◽  
Drug Induced Liver Injury ◽  
Hepatic Hydatidosis ◽  
Hepatocellular Damage ◽  
History Of

We report a case of a 47-year-old male, who was referred to the clinical hepatology services at Pablo Tobón Uribe Hospital for evaluation of a jaundice syndrome. After undergoing several exams, we diagnosed hepatic hydatidosis and the patient was treated with albendazole; however, after five months of uninterrupted treatment the patient again consulted and his liver test showed marked hepatocellular damage. This time, the patient was diagnosed with drug-induced liver injury due to albendazole, based on information from the clinical record, history of drug consumption, clinical and laboratory tests improved after discontinuing the medication and after discarding other possible causes; this diagnosis was supported by the CIOMS/RUCAM scale, which showed a “likely” correlation between hepatocellular damage and drug toxicity etiology.

Dementia with Lewy bodies

2020 ◽  
pp. 424-434
Author(s):  
Anto P. Rajkumar ◽  
Dag Aarsland
Keyword(s):  
Cognitive Impairment ◽  
Dementia With Lewy Bodies ◽  
Neuropsychiatric Symptoms ◽  
Clinical Manifestations ◽  
Lewy Bodies ◽  
Current Evidence ◽  
Future Research ◽  
Pharmacological Interventions ◽  
Neurodegenerative Dementia ◽  
History Of

Lewy bodies are eosinophilic spherical neuronal intracytoplasmic inclusions. Dementia with Lewy bodies (DLB) is the second most common neurodegenerative dementia. Clinical manifestations of DLB include cognitive impairment, extra-pyramidal symptoms, neuropsychiatric symptoms, and autonomic dysfunction. Studies investigating the epidemiology, pathophysiology, clinical diagnosis, and management of DLB have been exponentially increasing over the past two decades. This chapter begins with a brief history of DLB and its epidemiology. It provides an overview of the pathology of DLB, focusing on its neuropathology, neuroimaging, molecular biology, and genetics. The clinical presentation, diagnosis, differential diagnoses, and clinical course of DLB are presented. This chapter summarizes the current evidence for the pharmacological and non-pharmacological interventions of cognitive, neuropsychiatric, and other symptoms of DLB. Future research directives are highlighted at the end of this chapter.

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