1 / 25

The Basal Ganglia

The Basal Ganglia. Functional anatomy A. Input and output components cerebral cortex  BG  thalamus (VA)  frontal lobe. B. Parallel circuits C. Neurotransmitters D. Intrinsic circuitry of the basal ganglia and movement without. Regional anatomy A. Internal capsule and striatum

prem
Download Presentation

The Basal Ganglia

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  1. The Basal Ganglia

  2. Functional anatomy A. Input and output components cerebral cortex  BG  thalamus (VA)  frontal lobe. B. Parallel circuits C. Neurotransmitters D. Intrinsic circuitry of the basal ganglia and movement without. • Regional anatomy A. Internal capsule and striatum B. Series of coronal sections revealing anatomy and relationships of the nuclei. C. Midbrain sections showing substantia nigra.

  3. I. Functional anatomy Introduction: Basal ganglia are subcortical structures that are part of cerebral hemispheres. They receive input from and send regulatory signals back to the cortex (frontal lobes). Regulation of movement, cognitive, motivation, and emotion.

  4. A. Input and Output Components of the Basal Ganglia Know this figure!! VL

  5. The Striatum shown in relation to ventricles Note that caudate n. and putamen are connected by cell bridges (spanning internal capsule)

  6. B. Parallel circuits – anatomical “loops” subserve the various functions. Input-output nuclei specifically assigned to these ’jobs’ are outlined and specific frontal cortical projection areas are illustrated in Fig. 14-3.

  7. “Parallel circuits” Fig. 14-3 Skeletomotor loop: Control of skel muscle Oculomotor loop: Control of extraocular muscles Association loop: Role in cognition Limbic loop: Maturation/emotions

  8. Fig. 14-3 - Loops

  9. C. BG Neurotransmitters – used in the various BG circuits and outlined (Fig. 14-4) Glu/Asp: excitatory GABA: inhibitory (major neurotransmitter of the BG) Important neuromodulators: dopamine (from SN pc to striatum) acetylcholine (connect within striatum) enkephalin, substance P (out of striatum  direct + indirect pathways

  10. D. Intrinsic circuitry of the basal ganglia – and movement disorders. Refer to Box 14-1. Direct and indirect striatal output pathways: direct  excitatory to thalamus (VA) indirect  inhibitory to thalamic target neurons. Direct path: what happens when you inhibit an inhibitory signal (disinhibition = double negative)? Indirect path: opposite effect on thalamus (-) (and ultimately, cerebral cortex.

  11. Direct and indirect paths (Fig. 14-15) Indirect path: Note that the subthalamic n. is excitatory Inhibotory neurons from striatum (putamen)  external pallidal segments Filled: inhibitory; open, excitatory

  12. Double negative (disinhibition) excites the output of the STN, which will drive inhibitory output from Gpi SNr Thalamus {Internal segment of globus pallidus and SN pc} Therefore, the inhibition is increased  inhibitory output. This model helps us understand the mechanism of hypokinetic disorders (e.g., Parkinson’s Disease) and hyperkinetic disorders (e.g., Huntington’s Disease and hemiballism).

  13. Parkinson’s Disease: decreased dopamine from SN  decreased inhibition of the inhibition  excessive inhibitory output  classic signs of PD (hypokinesia, bradykinesia) – via decreased thalamic signals to cortex  decreased corticospinal outflow. Huntington’s Disease: decreased striatal (enkephalin) output and decreased inhibition of Gpo  enhanced excitatory effects of indirect path  decreased inhibition via direct path  hyperkinesis. Hemiballism: similar mechanism (subthalamic n. lesion).

  14. Parkinson’s: increased indirect

  15. Most modern therapies for PD have involved lesions without the circuit in an effect to re-established the balance (e.g., STN lesion)

  16. Hyperkinesis: increased direct

  17. II. Regional Anatomy • Internal capsule and striatum – recall how the striatum is divided into caudate n. and putamen by the anterior limb of the internal capsule and that cellular bridges (visible in horizontal section) exist between these (Fig. 14-6). Note also that internal and external segments of globus pallidus, posterior limb, and the thalamic nuclei below (Fig. 14-8). B. Series of coronal sections revealing anatomy of the nuclei and their spatial relationships.

  18. Horizontal Section Through Basal Ganglia (Fig. 14-6)

  19. Anterior section (Fig. 14-8) Note: head of caudate, nucleus accumbens, and cell bridges are prominent here. The head of caudate is often used as a radioligand landmark – normally buldges into anterior horn of lateral ventricles.

  20. Head of caudate = radiological landmark (Fig. 14-10)

  21. Fig. 14-11 The globus pallidus and ventral pallidum are beneath the anterior commissure.

  22. Subthalamic nucleus (Fig. 14-14)

  23. Mid-section

  24. Midbrain through the substantia nigra (Fig. 14-16).

More Related