Brain Clinical Correlations W. Rose 2011 Department of Kinesiology and Applied Physiology

You know what's wrong with me You know phrenology You saw my injury You can tell just by looking at my skull Contrecoup, on the rebound Contrecoup hurt me again And the second was worse by far than the first 'Cause it made me limerent When my head was hit I bounced away from it Or as someone who is craniosophic would say The brain went the opposite way Contrecoup, on the rebound Contrecoup hurt me again And the second was worse by far than the first 'Cause the first one woke my feelings for you But the contrecoup made my words untrue And it left me limerent Which is to say, how it goes Couched in terms no one knows And as if the choice were slim As if there's no synonym You know what's wrong with me You know phrenology You saw my injury You can tell just by looking at my skull Contrecoup, on the rebound Contrecoup hurt me again And the second was worse by far than the first Though the impulse is strong, the connection is weak And I know what to say, but forgot how to speak When it made me limerent Original radio version with story behind the song, is no longer available here as of here Department of Kinesiology and Applied Physiology Contrecoup Words and Music by John Linnell (TMBG)

Lumbar Puncture teaching video from NEJM Department of Kinesiology and Applied Physiology

Phineas Gage Macmillan, M. (2006). Restoring Phineas Gage: A 150th Retrospective. J. Hist. Neurosci. 9: Retrieved from On 13 September 1848, an explosion sent an iron rod rocketing through the head of Phineas Gage. He died in 1861 without being autopsied. Skull measurements were used to reconstruct a three-dimensional image of his brain and the trajectory of the rod. Pinpointing the lesion completes the historical record and restores Gage as a foundation for our contemporary understanding of the prefrontal cortices and their role in emotion, reason, and social behavior.

The Return of Phineas Gage: Clues About the Brain from The Skull of a Famous Patient. Normal brain fitted with the five pos- sible rods. The best rod is highlighted in solid white [except for (B), where it is shown in red]. The areas spared by the iron are high- lighted in color: Broca, yellow; motor, red; somatosensory, green; Wer- nicke, blue. (A) Lateral view of the brain. Numbered black lines corre- spond to levels of the brain section shown in (C). (D and E) Medial view of left and right hemispheres, respec- tively, with the rod shown in white. Damasio et al. (1994). Science 264:

Spontaneous Otogenic Pneumocephalus. Villa and Capdevila (2008). NEJM 358: e13. Department of Kinesiology and Applied Physiology

Pontine myelinolysis. Fleming and Babu (2008). NEJM 359: e29. A 26-year-old man with a history of chronic alcohol abuse presented with dysarthria, lethargy, and horizontal nystagmus. Results of a clinical examination and blood tests were otherwise normal, including a serum sodium level of 137 mmol per liter and serum osmolality of 287 mOsm per kilogram. Over the next 5 days, spastic quadriparesis [weakness of 4 limbs] and pseudobulbar palsy [functional impairment of cn IX-XII which control talking, eating, swallowing)]developed. Magnetic resonance imaging of the brain revealed central pontine myelinolysis with a well-defined lesion in the pons of low T 1 -signal intensity (Panel A, arrow) and high T 2 - signal intensity (Panel B, arrow). There was sparing of the ventral lateral and cortical spinal tracts and no space-occupying effect or distortion of the adjacent fourth ventricle. Central pontine myelinolysis is a noninflammatory, demyelinating condition commonly associated with the rapid correction of hyponatremia. However, it was originally described in those with chronic alcoholism and in malnourished persons. There is no specific treatment for central pontine myelinolysis, and this patient had no clinical improvement 6 months later.