Disorders of the Brainstem and Cerebellum

  • Larry E. DavisEmail author
  • Sarah Pirio Richardson


The chapter begins with discussion of anatomy and functions of the brainstem (mesencephalon, pons, and medulla) and cerebellum. No other part of the central nervous system is packed with so many critical axon tracts and nuclei. Main brainstem functions are as follows: to provide transit and processing nuclei for ascending and descending pathways that convey signals to and from the cerebellum, cerebrum, and spinal cord; to integrate functions such as consciousness, muscle tone, posture, and normal autonomic functions; and to house cranial nerves 3–10. The cerebellum occupies only 10 % of the brain volume but contains more neurons than the entire rest of the brain. Lesions in the brainstem often manifest as cerebellar, somatosensory and motor symptoms plus cranial nerve dysfunction. Damage to the cerebellum often results in errors in smooth motor movements. The chapter ends with a discussion of central pontine myelinolysis, lateral medullary syndrome or Wallenberg’s syndrome, and spinocerebellar atrophies with attention to their pathophysiology, major clinical features, major laboratory findings, and principles of management and prognosis.


Brainstem Cerebellum Central pontine myelinolysis Lateral medullary syndrome Wallenberg’s syndrome Spinocerebellar atrophy Mesencephalon Pons Medulla Ataxia Horner’s syndrome Hyponatremia 

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Recommended Reading

  1. Kandel ER, Schwartz JH, Jessell JM. Principles of neural science, 5th edn. New York: McGraw-Hill Professional; 2012. (Good review of brainstem and cerebellar anatomy and physiology)Google Scholar
  2. Querol-Pascual M. Clinical approach to brainstem lesions. Semin Ultrasound CT MRI. 2010;31:220–9. (Excellent brief review of brainstem locations for common brainstem clinical signs and symptoms)CrossRefGoogle Scholar
  3. Hurley RA, Filley CM, Taber KH. Central pontine myelinolysis: a metabolic disorder of myelin. J Neuropsychiatry Clin Neurosci. 2011;23(4):369–74. (Good review of the clinical manifestations and pathophysiology of CPM)PubMedCrossRefGoogle Scholar
  4. Kameda W, et al. Lateral and medial medullary infarction: a comparative analysis of 214 patients. Stroke. 2004;35:694–9. Comprehensive review of the features of medial vs. lateral medullary infarction with good anatomy-clinical correlations)PubMedCrossRefGoogle Scholar
  5. Durr A. Autosomal dominant cerebellar ataxias: polyglutamine expansions and beyond. Lancet Neurol. 2010;9:885–94. (Excellent review of clinical, pathological and genetic features of major SCAs)PubMedCrossRefGoogle Scholar

Copyright information

© Springer Science+Business Media, LLC 2015

Authors and Affiliations

  1. 1.Chief Neurology ServiceDistinguished Professor of Neurology New Mexico VA Health Care SystemAlbuquerqueUSA
  2. 2.Department of Neurology Health Sciences CenterUniversity of New MexicoAlbuquerqueUSA

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