Basal Ganglia anki deck

Basal Ganglia


  • Part of extrapyramidal system for movement (along with cerebellum)

  • Contributes to behaviour, motor and cognition

  • Related to movement and neuropsychiatric disorders - Thalamus is relay station for ascending info


    • Striatum = caudate and putamen • Receiving station/input centre of basal ganglia
      • Caudate has a more extensive connection with cortex compared to putamen • Parkinsons
      • Cortico-striate pathway
    • Lentiform nucleus = globus pallidus and putamen
      • Target for Wilson’s disease
      • Lenticuostriatal artery (branch of MCA) blood supply
    • From lateral to medial: putamen —> GPE —> GPI
    • Substantia nigra: - Pars compacta = dopaminergic - Nigro-striate pathway Amygdala
  • Tail of caudate is connected to amygdala and is involved with emotion



    • Globus pallidum interna and substantia nigra reticulata are the 2 major output stations
    • Goes to VA & VL of thalamus Pathway
    • Glutamate activates inhibitory neurons in striatum which turn off the globus pallidus interna
    • Inhibiting the inhibitor globus pallidus interna so then the thalamus is active
    • indirect — reactivated globus pallidus inhibitory neurons to turn the thalamus back off again
    • When dopamine binds D1, it turns on the direct
    • When dopamine binds to D2, it turns off the indirect
    • Ach makes D2 less sensitive to dopamine to restore the inhibition on movement
    • Pars compacta is where the dopaminergic neurons are
    • Indirect overactive or direct underactive = hypokinetic; parkinsons
    • Direct overactive or indirect underactive = hyperkinetic; huntingtons, hemiballismus, wilsons disease Action/Motor Functions
    • Gatekeeper for movements and muscle tone
    • Suppresses unwanted movements (indirect) and only allows required movements (direct)
    • Secondary movements such as arm swing
    • Stereotyped movements such as laughing
    • Semiautomatic movements
    • Supporting movements


Behaviour Functions

  • Lack of initiative to perform movements (akinesia); seen in parkinsons

• Manifests as hypokinesia and mask-like expressionless face Cognitive Functions

    • Caudate plays an important role in learning of sequential non-declarative motor skills (learning to ride a bike)
    • Hippocampus is involved in episodic/declarative memory
    • Loss of non-declarative memory in basal ganglia lesion = able to remember trying to do a mirror drawing before but difficulty in learning the skill
    • Loss of declarative memory in hippocampus lesion = cannot remember trying to draw before but is able to learn the skill of mirror drawing Neurons in CNS Most Vulnerable to Anoxic Death (Long Axons) - Pyramidal neocortical neurons
  • Purkinje neurons of cerebellum
  • Pyramidal neurons of hippocampal CA1 - Spiny neurons of striatum Parkinsons
    • TRAP: tremors (resting), rigidity, akinesia, postural (stooped) and gait disturbances (festinating)
    • Late dementia, usually subcortical
    • Lead-pipe rigidity/cog-wheel rigidity/plasticity = no loosening, resistance throughout, tremors superimposed on rigidity. SEEN IN PARKINSONS.
    • Clasp-knife rigidity/spasticity = resistance at first but tone loosens on extension. SEEN IN UMN LESIONS.


    • Signs are contralateral to the lesion and begin unilaterally. As it advances, will become bilateral.
    • Posture is last to be affected
    • Micrographia: diminished letter size with writing
    • Pathology: degeneration of dopamine neurons in substantia pars compacta • Replaced by eosinophilic lewy bodies that may contain synuclein, ubiquitin Huntington’s Disease
    • Caudate nucleus atrophy —> putamen —> cortex
    • MRI will show bilateral caudate atrophy with hydrocephalus ex vacuo
    • Death by 6th decade
    • CP: middle aged with signs of dementia, choreiform movements starting in fingers and toes, dysphagia, grimacing
    • Choreiform movements: rapid, jerky, non-repetitive pseudopurposive movements
    • Dementia, subcortical type. Difficulty learning skills.
    • Neuropsychiatric: forgetfulness, impulsivity, irritability, poor concentration and other emotional or behavioural disturbances at the beginning progressing to anxiety, depression, mania and suicide
    • AD, chromosome 4
  • family hx of movement/psychiatric disorders
    • CAG repeats encoding for glutamine >36; turns its RNA in the HTT gene cytotoxic
    • Genetic anticipation
    • Abnormal huntingtin is apoptotic Sydenhams Chorea
  • Autoimmune response to GAS beta-hemolytic - Girls aged 5-15 in developing countries


    • Pathophysiology: cross reactivity of strep antigens and membrane proteins of striatal neurons; host antibodies attack bacteria and striatal neurons —> transient chorea that causes inflammation but doesn’t kill the neurons
    • Initially presents as pharyngitis
    • ARF after 1-5 weeks (fever, joint pain, rash, cardiac)
    • 1-6 months after infection, will develop dance-like choreatic movements which disappear with sleep and worsen with stress
    • May be restless, aggressive or emotional
    • Self-limiting
    • Caudate nucleus is implicated but it is not long-lasting or degenerative
    • Chorea gravidarum: some with childhood sydenham’s chorea develop chorea during 2nd trimester of pregnancy Hemiballismus
    • High-amplitude rapid, flinging, flailing (ballet-like) unilateral involuntary movements
    • Lesion of contralateral subthalamic nucleus (lacunar infarct; lenticulostriate arteries from HTN or diabetes)
    • Causes exhaustion or injury Wilson’s Disease
    • Error in copper metabolism; deficiency of ceruloplasmin and decreased copper elimination
    • AR ATP7B mutations
    • Copper is used by dopaminergic neurons
    • Hepatolenticular degeneration: copper deposits in liver, lenticular nuclei (mostly putamen) and eyes
    • <30 age onset
    • Hepatic presentation: jaundice, hepatomegaly, edema, ascites


  • Neuro presentation: dysarthria, dystonia, rigidity, wing-beating tremor, chorea, sardonic smile, gait abnormalities, ataxia

  • Psychiatric: irritability, impulsivity, anxiety, depression, substance misuse - Ocular: Kaiser-Fleischer ring, sunflower cataracts

Tourette Syndrome

    • Premonitory urge followed by motor/phonic tics, coprolalia (explosive/vulgar swearing)
    • Increased dopamine activity
    • M:F = 3:1
    • 3-8 years
    • Tics must be present for >1 year and onset before age of 21 - Tics can be suppressed - Comorbid with ADHD, OCD, ASD Extrapyramidal Reactions
    • Akathisia: inner restlessness, inability to keep still (rocking, pacing, fidgeting) within 2 weeks of starting neuroleptics. May also present with anxiety and dysphoria.
    • Acute Dystonic Reaction: spasms of jaw, face, neck muscles within 5 days of starting neuroleptics. May also present with dysphagia.
    • Perioral Tremor (Rabbit syndrome): abnormal orofacial lips, mouth and jaw movement BUT NO TONGUE INVOLVEMENT after months-years of antipsychotics - Responds well to anti-parkinson drugs - Usually not permanent
    • Tardive Dyskinesia: choreiform movements of face and trunk, dystonia, tics - Mostly irreversible and persistent - TONGUE PROTRUSIONS - Worsened by anti-parkinson drugs


  • D/t long term antipsychotic medications - Supersensitivity of dopamine receptors

Movement Disorders Overview

  • Dyskinesia: abnormal movement usually due to lesions in basal ganglia

  • Can be bradykinesia, hypokinesia, akinesia, or hyperkinesia

    • Lesions in basal ganglia present contralaterally
    • Rigidity
    • Dystonia = slow or sustained distorted positioning
    • Athetosis: proximal writhing or twisting
    • Chorea: continuous jerky “dance”
    • Choreoathetosis: merging chromatic and athetotic
    • Ballismus: high amplitude flinging
    • Tics: sudden, brief action preceded by an urge and followed by relief

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