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Related Concept Videos

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Glutamate is a fundamental neurotransmitter in the central nervous system, playing a vital role in neuronal communication and various cognitive processes. Glutamate stands as the principal excitatory neurotransmitter in the brain. Its presence is crucial for the communication between neurons, underpinning essential processes such as synaptic transmission, neuronal excitability, and plasticity. These functions are vital for higher-order cognitive processes, including learning and memory. The...
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Antiepileptic Drugs: GABAergic Pathway Potentiators01:18

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γ-aminobutyric acid or GABA, plays a pivotal role as an inhibitory neurotransmitter in the brain. GABA pathway potentiators, also known as GABAergic drugs, are a class of pharmaceutical agents designed to enhance the functioning of the GABAergic system. These medications primarily treat epilepsy, a neurological disorder characterized by recurrent seizures.
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Long-term depression, or LTD, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTD is the process of synaptic weakening that occurs over time between pre and postsynaptic neuronal connections. The synaptic weakening of LTD works in opposition to synaptic strengthening by long-term potentiation (LTP) and together are the main mechanisms that underlie learning and memory.
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Learning disabilities are cognitive disorders caused by neurological impairments that affect cognitive functions like language and reading, without indicating overall intellectual or developmental challenges. These disabilities differ from global intellectual or developmental disabilities as they are limited to distinct cognitive functions. Common learning disabilities include dysgraphia, dyslexia, and dyscalculia, each of which impacts unique aspects of learning.
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Lamotrigine-Associated Progressive Dysphasia and Cognitive Dysfunction.

Joshua C Brown1,2, Jessica L Broadway2

  • 1Warren Alpert Medical School of Brown University, 345 Blackstone Blvd, Providence, RI, USA.

OBM Neurobiology
|April 24, 2023
PubMed
Summary
This summary is machine-generated.

Lamotrigine, usually well-tolerated, caused a severe dementia-like condition in a patient. This neuropsychiatric syndrome reversed upon lamotrigine dose reduction, highlighting a rare adverse effect.

Keywords:
Reversible cognitive dysfunctionanticonvulsant adverse effectsencephalopathyhyperreflexialamotrigine adverse effectslanguage disordermyoclonusorganic mental disordersparaphasiastoxicity at approved dose

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Area of Science:

  • Neuroscience
  • Clinical Pharmacology
  • Geriatric Medicine

Background:

  • Lamotrigine is widely prescribed and generally considered safe with minimal cognitive impact.
  • Adverse neuropsychiatric events associated with lamotrigine are uncommon, especially at standard therapeutic doses.

Purpose of the Study:

  • To report a rare case of severe, reversible dementia-like syndrome linked to lamotrigine.
  • To document the clinical, electrophysiological, and neuroimaging findings in this unique presentation.

Main Methods:

  • A 62-year-old female patient presented with rapid cognitive decline.
  • Clinical examination, electroencephalogram (EEG), and fluorodeoxyglucose-Positron Emission Tomography (FDG-PET) were utilized.
  • Lamotrigine dosage was reduced, and outcomes were monitored.

Main Results:

  • The patient exhibited global cognitive impairment, ataxia, Wernicke-like dysphasia, and hyperreflexia with clonus.
  • EEG showed burst suppression, and FDG-PET revealed bilateral parietal hypometabolism.
  • Symptoms completely resolved after lamotrigine dose reduction.

Conclusions:

  • This case represents the first documented instance of a severe neuropsychiatric syndrome attributed to standard-dose lamotrigine, unrelated to epilepsy.
  • Clinicians should consider lamotrigine as a potential cause of unexplained cognitive decline and neurological symptoms.
  • The findings underscore the importance of medication review in patients presenting with acute neurological deterioration.