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Basal Ganglia

Basal Ganglia Anatomical Review

Basal Ganglia Anatomical Grouping

Basal Ganglia

Basal Ganglia Direct and Indirect Pathways

Basal Ganglia Loops

Figure 1

Basal Ganglia Loops

Basal Ganglia Somatotopic Organization

7 Concepts for The Rate Model

Basal Ganglia Indirect Pathway

Motor Tic Disorder

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Sydenham’s Chorea

Hemichorea--Hemiballism after Diabetic Ketoacidosis

Basal Ganglia Direct Pathway

Figure 3

Young Onset Parkinson’s Disease

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Parkinson’s Feature of Re-Emergent Tremor

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Video Examples

Unified Parkinson’s Disease Ra%ng Scale

•  Hand Movements •  O = Normal •  1 = mild slowing, and/or reduc,on in amplitude •  2 = moderately impaired, definite and early fa,guing, may have occasional arrests

•  3 = severely impaired, frequent hesita,ons and arrest •  4 = can barely perform

Basal Ganglia Hyperdirect Pathway

Neurodegenerative Diseases of the Basal Ganglia

Lewy body disease in Parkinson’s

Parkinson disease, Lewy body: The Lewy body is the pathological hallmark of Parkinson disease. The Lewy body inclusion shows an eosinophilic core surrounded by a pale halo (arrow). The protein alpha-‐synuclein is a component of the Lewy body.

Degenerative Substantia Nigra in Parkinson’s Disease

The lea shows Parkinson's disease with a pale substan,a nigra compared to a normal ,ssue on the right

Genetic Neurodegenerative Disorder – Hunington’s Disease

Microscopically, the caudate nucleus in Hun,ngton's disease demonstrates loss of neurons along with gliosis.

Hun,ngton's disease is shown grossly in this coronal sec,on of the brain. It demonstrates atrophy of the caudate with resultant increase in size of lateral ventricles.

Lacunar Infarction of the Basal Ganglia

Lacunar infarct (<1cm): A rela,vely small cys,c lesion in the putamen secondary to small vessel disease. Common loca,ons for lacunes include basal ganglia, pons, internal capsule, thalamus and cerebral white maSer.

Lacunar Infarcts

Mechanisms that Injure the Basal Ganglia

Poewe W, Djamshidian-‐Tehrani A. Movement disorders in systemic diseases. Neurol Clin. 2015 Feb;33(1):269-‐97.

Carbon monoxide poisoning: During the first few hours aaer carbon monoxide poisoning, the brain is swollen, congested and cherry-‐red. Aaer 24-‐48 hours of survival, scaSered petechial hemorrhages may be seen in white maSer with larger hemorrhages in the pallidum (arrows).

Pesticide Induced Destruction of Basal Ganglia

Infectious Destruction of Basal Ganglia

Immune Cross-Reactivity of the Basal Ganglia – PANDAS

(Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcus)

Iron Accumulation Induced Destruction of the Basal Ganglia

Globus Pallidus Iron Accumulation

Copper Toxicity (Wilson’s Disease) Destruction of the Basal Ganglia

Wilson disease (hepatolen%cular degenera%on): Wilson disease is an autosomal recessive disorder caused by muta,ons in a copper transport gene (ATP7B). The putamen appears brown and shrunken. The caudate is oaen severely affected, but pallidum, thalamus and brain stem may be less severely involved.

Autoimmune Destruction of Basal Ganglia

Basal Ganglia and Nutritional Considerations

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