Sunday 23 March 2014

Mamillary body compression by Basilar Presenting as Parkinson's Clinically

A 50 y o male comes for MRI Brain.
In history technician mentions recent onset impaired memory and confusion. Clinical diagnosis of Parkinson disease noted in the accompanying referring letter.

MRI Brain sagittal and axial T2 w images show flow void of abnormally high riding basilar tip_ a normal anatomical variation but significant in this case as it is causing obvious compression over mamillary bodies explains patients problem with memory and may explain Parkinson’s presentation.


Mammillary body anatomy 
The mammillary bodies are a pair of small round bodies, located on the under surface of the brain as a part of the diencephalon and form part of the limbic system. They consist of two groups of nuclei, the medial mammillary nuclei and the lateral mammillary nuclei.
Neuroanatomists have often categorized the mammillary bodies as part of the hypothalamus.

Role of mammillary bodies in memory
Mammillary bodies, and their projections to the anterior thalamus via the mammillothalamic tract, are important for recollective memory. The medial mammillary nucleus is mainly responsible for the spatial memory deficits that are seen in rats with mammillary body lesions. They are believed to add the element of smell to memories.
Damage to the mammillary bodies due to thiamine deficiency is implied in pathogenesis of Wernicke-Korsakoff syndrome. Symptoms include impaired memory, also called anterograde amnesia, suggesting that the mammillary bodies may be important for memory. Mammillary body atrophy is present in a number of other conditions, such as colloid cysts in the third ventricle, Alzheimer’s disease, schizophrenia, heart failure, and sleep apnea. In spite of this the exact function of the mammillary bodies is still not clear.

Role of hypothalamus in Parkinson disease.
Sandyk R, Iacono RP, Bamford CR.

It is currently believed that Parkinson disease (PD) is due to a degenerative process that independently damages multiple areas of the central and peripheral nervous system. Loss of nigrostriatal dopamine is now widely recognized as being directly related to the motor symptoms in Parkinson's disease. Parkinsonian patients also exhibit symptoms and signs suggestive of hypothalamic dysfunction (e.g. dysautonomia, impaired heat tolerance). The latter clinical features are supported by pathological, biochemical and endocrinological findings. Lewy body formation has been demonstrated in every nucleus of the hypothalamus, specifically the tuberomamillary and posterior hypothalamic. Preferential involvement of the hypothalamus was also noted in patients after post-encephalitic parkinsonism. Loss of dopamine (30-40%) in the hypothalamus of affected patients has been shown in recent studies, and is compatible with the reported abnormalities of growth hormone release in response to L-dopa administration, elevated plasma levels of MSH, and reduced CSF levels of somatostatin and beta-endorphins in these patients. Deranged immunological mechanisms have been found in PD patients including the presence of autoantibodies against sympathetic ganglia neurons, adrenal medulla and caudate nucleus. On the evidence of on pathological studies demonstrating the early vulnerability of the hypothalamus in aging and PD, and the known role of the hypothalamus in immune modulation, we expect that it will be shown that primary damage of the hypothalamus leads to subsequent secondary degeneration of structures receiving direct projections from the hypothalamus.

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