1. Considering the patient’s history and physical examination, how precisely can the neurologic lesion be localized in this case?
Not very precisely (see below and see slide #1)
2. Does this patient’s left facial weakness indicate a lower motor neuron or upper motor neuron process?
Upper motor neuron facial weakness
3. Indicate the structures involved by the pathologic process to produce this patient’s mild left-sided hemiparesis, hyperreflexia, extensor plantar reflex, and left UMN facial weakness. If precise localization is not possible, list as many levels or structures as you can that might produce the same clinical picture.
Right corticospinal and corticonuclear (corticobulbar) tracts above the lower third of the pons
4. Indicate the structures involved by the pathologic process to produce this patient’s mild left-sided numbness and tingling of the face, arm, and leg. If precise localization is not possible, list as many levels or structures as you can that might produce the same clinical picture.
Right medial, spinal, & trigeminal lemnisci above the mid-pons, right VPM/VPL nuclei of the thalamus, right posterior limb of internal capsule, right postcentral gyrus
5. Indicate the structures involved by the pathologic process to produce this patient’s left-sided findings on cerebellar examination (i.e., impaired finger-to-nose, heel-to-shin, dysdiadochokinesia). If precise localization is not possible, list as many levels or structures as you can that might produce the same clinical picture.
Left cerebellar hemisphere, left superior cerebellar peduncle (SCP) below (or right SCP above) the inferior midbrain, right VL nucleus of the thalamus, right thalamocortical radiations, right precentral gyrus or premotor area, right frontopontine tracts, right pontine nuclei in the basilar part of the pons
6. Discuss the “localization of the lesion” in this case.
It is difficult to localize the lesion in this case and in this syndrome. Basically, this syndrome can be caused by a fairly discrete lesion at any location where the corticospinal fibers and the neocerebellar (cortico-ponto-cerebellar) pathways lie in close approximation. The usual lesions (in a case such as this) would be in the right base of the pons, right cerebral peduncle involving the pyramidal tract in the crus cerebri and the superior cerebellar peduncle (SCP) after its decussation, and the right posterior limb of the internal capsule involving the pyramidal tract and the thalamocortical radiations and/or the frontopontine fibers.
7. The findings in this case represent a classic neurologic syndrome. What is the name of that syndrome, and what is its usual cause?
Ataxic hemiparesis. Lacunar infarct (variable locations, as above)
8. In general, what type of pathologic process do you think is involved in this case?
Vascular – Lacunar infarct is most common.
In this patient, the lesion was a small thalamic intracerebral hematoma, involving the right VL nucleus of the thalamus to produce the neocerebellar findings. The mild left hemiparesis was probably caused by edema involving the adjacent posterior limb of the internal capsule. Lastly, the mild left-sided sensory findings were probably caused by edema or slight direct involvement of the VPL/VPM nuclei of the thalamus. This sensory involvement is not typical of the syndrome of ataxic hemiparesis, but it may be the only clue in this case to suggest the localization of the lesion to the thalamus.
9. What diagnostic procedure(s) would you undertake at this point?
References:
1. Fisher CM, Cole M. J Neurol Neurosurg Psychiatry 1965;28:48-55.
2. Koppel BS, Weinberger G. Eur Neurol 1987;26:211-215.
3. Nabatame H, Fukuyama H, Akiguchi I, et al. Ann Neurol 1987;21:204-207.
4. Helweg-Larsen S, Larsson H, Henriksen O, Sorensen PS. Neurology 1988;38:1322-1324.
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