Neuroanatomy - Connections Of The Basal Ganglia

  • Uploaded by: Patricia Sio
  • 0
  • 0
  • August 2019
  • PDF

This document was uploaded by user and they confirmed that they have the permission to share it. If you are author or own the copyright of this book, please report to us by using this DMCA report form. Report DMCA


Overview

Download & View Neuroanatomy - Connections Of The Basal Ganglia as PDF for free.

More details

  • Words: 600
  • Pages: 3
Chapter 10: The Basal Nuclei (Basal Ganglia) and their Connections Connections of the Corpus Striatum Afferent Fibers Corticostriate Thalamostriate Nigrostriate Brainstem Striatal

Efferent fibers Striatopallidal Striatonigral

Input All parts of the cerebral cortex (largest from sensorymotor cortex) Intralaminar nuclei of the thalamus Neurons in the substantia nigra Ascending fibers from the brainstem

Output

Neurotransmitter Glutamate

Caudate nucleus and the putamen Dopamine Serotonin

Input Output Caudate nucleus and Globus pallidus putamen Substantia nigra

Neurotransmitter GABA GABA/Acetylcholine or substance P

Connections of the Globus Pallidus Afferent fibers Striatopallidal

Input Caudate nucleus and putamen

Efferent fibers Ansa leticularis Fasciculus lenticularis Pallidofugal Pallidotegmental fibers Pallidosubthalamic fibers

Output Globus pallidus

Input

Neurotransmitter GABA

Output Thalamic nuclei Subthalamus

Globus pallidus

Caudal tegmentum of the midbrain Subthalamic nuclei

The activity of the basal nuclei is initiated by information received from the premotor and supplemental areas of the motor cortex, the primary sensory cortex, the thalamus, and the brainstem. The outflow from the basal nuclei is channelled through the globus pallidus, which then influences the activities of the motor areas of the cerebral cortex or other motor centers in the brainstem.

Chorea

Disorders Huntington’s disease

 Involuntary, quick, jerky, irregular, nonrepetitive movements (e.g., swift grimaces, sudden movement of the head or limbs)

Cause Single gene defect on chromosome 4 which encodes  Autosomal dominant for the protein huntingtin  Onset most often in (unknown function). CAG adult life (encodes for glutamine) is  Death 15-20 years repeated many more times after onset than normal.

Manifestation  Choreiform movements  Progressive dementia Degeneration of the neurons of the striatonigral-inhibiting pathway  neurons of substantia nigra become overactive  nigrostriatal pathway inhibits the caudate nucleus and putamen  abnormal movements Degeneration of the caudate nuclei  enlarged lateral ventricles

antigens of the Sydenham chorea The streptococcal bacteria are (St. Vitus’ dance) similar in structure to the  Disease of childhood proteins present in the  Rapid, irregular, membranes of striatal involuntary neurons. The host’s antibodies movements of the not only combine with the limb, face, and trunk bacterial antigens but also  Associated with attack the membranes of the rheumatic fever neurons of the basal ganglia. Lesion (usually a small stroke) Hemiballismus in the opposite subthalamic nucleus or its connections.  Progressive disease of Parkinson Disease (Primary Parkinsonism unknown cause  Commences between ages 45-55 years old  Most common type of parkinsonism found in clinical practice  Associated with neuronal degeneration in the substantia nigra and, to a lesser extent, in the globus pallidus, putamen, and caudate nucleus

Choreiform movements are transient; there is full recovery

Involuntary movement confined to one side of the body  Tremor – result of the alternating contraction of agonists and antagonists  Rigidity  Bradykinesis  Postural disturbances  No loss of muscle power; no loss of sensibility Since the corticospinal tracts are normal, the superficial abdominal reflexes are normal, and there is no Babinski response. The deep tendon reflexes are normal.

Degeneration of substantia nigra  reduction in release of dopamine within the corpus striatum  hypersensitivity of the dopamine receptors in the postsynaptic neurons in the striatum Drug-induced Parkinsonism

Postencephalitic parkinsonism Iatrogenic parkinsonism Atherosclerotic parkinsonism Athetosis

Drugs that block striatal dopamine receptors (D2) (e.g., phenothiazines and butyrophenones). Drugs that may deplete striatal dopamine (e.g., tetrabenazines). Damage in basal nuclei due to viral encephalitis Side effect of antipsychotic drugs (e.g., phenothiazines) Occurs in elderly hypertensive patients Degeneration of the globus Slow, sinuous writing pallidus. movements that most commonly involve the distal segments of the limbs

It is in the subthalamic nucleus that smooth movements of different parts of the body are integrated.

Related Documents

Basal Ganglia
November 2019 18
Basal Ganglia
July 2020 18
Lab Basal Ganglia
November 2019 17
Basal Ganglia Handout Battag
November 2019 20
The Basal Ganglion
December 2019 10

More Documents from "Examville.com"