Etoh-related neurological disorders

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Alcoholic cerebellar degeneration

  • A common type of acquired cerebellar ataxia characterized by chronic vermian atrophy cerebellar degeneration
  • Aka:
    • Alcohol-related cerebellar degeneration
    • Alcohol-induced cerebellar degeneration
    • Nutritional cerebellar degeneration
  • Duration of abuse is more important than amount used
  • Prevalence is estimated at 12 – 27% from autopsies
  • Clinical features
    • Gait ataxia (Main)
      • Due to involvement of the anterosuperior cerebellar vermis
    • Coarse tremor
    • Truncal instability
    • Nystagmus
    • Lower limb ataxia
    • Upper limb ataxia (in severe cases)
  • Mechanism
    • Alcohol neurotoxicity AND
    • Nutritional deficiency (notably thiamine)
  • Pathology
    • A variable loss of the molecular layer and granule cells
      • Purkinje cell loss in the cerebellar cortex
      • Bergmann gliosis
    • Associated neuronal loss in the dorsal inferior olivary nuclei may also be present.
    • Underlying cerebellar white matter is otherwise preserved
  • Imaging
    • Best seen in MRI T1
        • Cerebellar volume loss
          • Localized to the anterior superior vermis (lingula, central lobule, culmen, declive)
          • Associated widening of inter-folial sulci.
        • Subsequent progression to involve the posterior inferior vermis and anterior lobes of the cerebellum can occur
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Alcoholic hallucinosis

  • Prevalence of 0.6-0.7% in alcoholics
  • A rare complication of chronic alcohol abuse
  • Predominantly auditory hallucinations that occur either during or after a period of heavy alcohol consumption
  • Hypo function of thalamus

Alcoholic neuropathy

  • Most common adverse effects of chronic alcohol consumption.
    • 25% to 66% of chronic alcohol users experience some form of neuropathy
  • Damage to the nerves due to the direct toxic effect of alcohol and the malnutrition. (thiamine, vitamin-B1 deficiency
  • Clinical presentation - Lower limb
    • Pain
    • Ataxia
    • Parasthesias
  • More than 100 g/day over a number of years was likely to cause peripheral neuropathy

Alcohol withdrawal seizures

  • Mechanism
    • Ethanol
      • At lower dose
        • Is a central nervous system depressant that produces euphoria and behavioral excitation
        • Due to increased glutamate binding to N‐methyl‐D‐aspartate (NMDA) receptors;
      • At higher dose
        • Leads to acute intoxication
        • By potentiation of the GABA effects
          • Particularly GABA receptors with delta subunits.
    • Abrupt cessation of chronic alcohol consumption unmasks these changes with a glutamate‐mediated CNS excitation resulting in autonomic overactivity and neuropsychiatric complications such as delirium and seizures.
    • The latter are usually of generalized tonic–clonic type and are mediated largely in the brainstem by abrogation of the tonic inhibitory effect of the GABAergic delta subunits.
      • Therefore, the trigger zone of these seizures is distinct from that believed to be responsible for seizures in the context of epilepsy, and this may explain why epileptiform activity is rarely observed in the EEG after alcohol withdrawal seizures.
    • As upregulation of NMDA receptors as well as reduced GABA‐A receptor inhibition largely explain the clinical symptoms, the therapeutic approach to AWS mainly targets these mechanisms.

Beriberi

  • Vitamin B1 (Thiamine) deficiency
  • Dry beriberi
    • Polyneuropathy, symmetric muscle wasting
  • Wet beriberi
    • High-output cardiac failure (due to systemic vasodilation)

Delirium tremens

  • 3% to 5%
  • Exhibit symptoms of severe alcohol withdrawal
    • Profound confusion
    • Autonomic hyperactivity
    • Cardiovascular collapse
  • Treatment Benzodiazepines

Marchiafava-Bignami disease

  • Lesions can appear as hypodense regions of the corpus callosum on tomography, and as areas of diminished
  • T1 signal and increased T2 signal on magnetic resonance. Also, an interhemispheric disconnection syndrome has been found in survivors.
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Tobacco-alcohol amblyopia

  • Painless bilateral loss of vision in association with alcohol abuse.
  • Due to damage to macula

Korsakoff syndrome

  • Amnestic disorder due to chronic alcohol overuse;
  • Clinical features
    • Confabulation
    • Personality changes
    • Memory loss (permanent)

Wernicke’s encephalopathy

  • Acute, reversible, life-threatening neurologic condition.
  • Symptoms: (CorONA beer)
    • Confusion,
    • Ophthalmoplegia/Nystagmus,
    • Ataxia

Wernicke-Korsakoff syndrome

  • Damage to medial dorsal nucleus of thalamus, mammillary bodies.
  • Presentation is combination of Wernicke encephalopathy and Korsakoff syndrome.