I. Function: modulates thalamic output to motor cortex to plan, execute and terminate smooth movements.
II. Components:
a. (Neo)Striatum
– consists of Caudate
(lateral to the lateral ventricles) and Putman
b. Globus Pallidus – consists of Globus Pallidus Externa (GPe)
and G. P. Interna (GPi)
c. Substantia Nigra
– consists of Substantia nigra pars compacta (SNc) and S. N. pars reticulata (SNr)
d. Subthalamic nuclei
III. Neurophysiology:
a. Input of striatum is mostly excitatory (Glutamate) from cortex and thalamus.
Exception: Input from SNc is dopaminergic, can cause overall 1) excitation of GPe 2) inhibition of GPi
b. Output of striatum is mostly inhibitory (GABA)
i. GPi – its ouput is also inhibitory, to dorsal thalamus, which normally is excitatory to motor cortex.
ii.
GPe – it inhibits subthalamic nuclei, which normally is excitatory to
GPi.
*Note: the so called “indirect pathway”
according to Dr. Hitchcock, begins with the inhibition of GPe, so the effect of the indirect pathway, and the
result of “over-activation” of GPe are not the same but exactly
opposite. Same goes for
“direct pathway” and GPi.
c. Output of GPi and SNr is mostly inhibitory (GABA) to dorsal thalamus.
d. Output of dorsal thalamus is excitatory (Glu) to motor cortex.
Overall effect of the direct pathway, i.e. inhibition of GPi, on motor cortex is excitatory.
Overall effect of the indirect pathway, i.e. inhibition of GPe, on motor cortex is inhibitory.
*For those that find it confusing, my apology, and the three diagrams on neuro course packet p.253 may be helpful.*
IV. Clinically relevant lesions:
a. Substantia Nigra – Parkinson’s disease
-loss of dopaminergic neurons
-excessive
inhibition of GPe (or over-active indirect pathway, see III.b.ii) – Hypokinesia
b.Striatum – Huntington’s disease
-release inhibition of GPe, excess inhibition of of subthalamic nuclei
-excessive
inhibition of GPi (or over-active direct pathway) -- Hyperkinesia
c.Globus pallidus – inability to maintain postural support.
d.Subthalamic nuclei
– Hemiballism
Source: Lecture notes 2/12/2001 (Hitchcock), BRS Physiology p.58-59.
11. Clinical exam of pupillary light reflex: pathway tested, important anatomic lesions, swinging light test.
I. “Swing light test” according to Dr. Trobe
– “1) with patient fixating on a distant object in a dark room,
shine the flashlight in the right eye, noting the degree of pupillary
constriction, 2) swing the light to shine in the left eye, noting its degree of
constriction, if it dilates (or constricts less than the right pupil), this
is a left afferent pupillary defect, 3) if
the left pupil constricts, swing the light back in the right eye, if
it dilates, this is a right afferent pupillary defect.
II. Pathway:
Input: retina (unilateral) à optic n. à
optic chiasm à Superior Colliculus à
Integration (bilateral) Edinger-Westphal
nuclei (parasympathetic, aka accessory oculomotor nuclei of CN III) à
Output: CN III à ciliary ganglion à
Pupillary sphincter muscle
III.Findings:
The amount of light shines in two eyes are distributed equally (integrated together), and reflexively, both pupils should normally constrict equally. When the degree of constriction changes when the same amount of light is changed from one eye to another, the most likely explanation is that there is a lesion affecting the light input, between the retina and the optic chiasm, where the light input is strictly unilateral. Lesions after the chiasm will not affect the light reflex because the input has become bilateral.
Source: Lecture notes, 3/20/2001.