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 was head was hit
I bounced away from it
Or as someone who was 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 just left me feeling inert
But the contrecoup woke my feelings for you
And it left me limerent
Words and Music by John Linnell (TMBG)
Link to Real Audio
0:50-1:20, 2:35-4:00, 5:44-6:15
Lumbar Puncture teaching video from NEJM
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Phineas Gage. 1848.
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.
Macmillan, M. (2006). Restoring Phineas
Gage: A 150th Retrospective. J. Hist.
Neurosci. 9: 46-66. Retrieved 2009-1113 from http://joeltalks.com.
The Return of Phineas
Gage: Clues About the
Brain from The Skull of a
Famous Patient.
Normal brain fitted with the five possible 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 highlighted in color: Broca, yellow; motor,
red; soma- tosensory, green; Wernicke, blue. (A) Lateral view of the
brain. Num- bered black lines correspond to levels of the brain section
shown in (C). (D and E) Medial view
of left and right hemispheres, respectively, with the rod shown in white.
Damasio et al. (1994). Science 264:
1102-1105.
Spontaneous Otogenic Pneumocephalus. Villa and Capdevila (2008). NEJM 358: e13.
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 T1-signal intensity (Panel A, arrow) and high T2signal 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.