Anesthesiology:
doi: 10.1097/ALN.0000000000000164
Correspondence

In Reply

Leffert, Lisa R. M.D.; Schwamm, Lee H. M.D.

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The authors wish to thank Dr. Derakhshan for his detailed letter in response to our review,1 and for reminding the readers that the phenomenology of herniation is complex and may vary between individuals. In his letter, he calls attention to the first descriptions by Kernohan of the falsely localizing hemiparesis; in several cases of patients with supratentorial intracranial lesions and mass effect, the neurologic impairment was found ipsilateral to the side of hemispheric injury rather than the usual contralateral location. This was thought to be due to descent of the ipsilateral uncus of the temporal lobe pushing the brainstem contralateral rather than downward, with a resulting notching of the crus cerebri against the contralateral cerebellar tentorium.2,3 These findings were of greatest importance in the preimaging era when neurosurgeons needed to be persuaded by clinical findings alone as to which side of the skull to place a burr hole or larger craniotomy.4
Although the etiology of ipsilateral versus contralateral symptoms and whether the cause is vertical versus lateral displacement of brain tissue are still not fully elucidated,2–5 it is important to note that these signs of neurologic impairment are in no way false and are generally harbingers of significant pathology. Our article attempts to provide the reader with an understanding of how to assess the risk of herniation in patients with differing types of intracranial pathology, and the impact of neuraxial anesthetics in these cases. It does not address the varied neurologic manifestations of brain herniation, which, itself, is the proper subject of a dedicated review.
Specifically, we would like to remind the reader against maneuvers that will acutely lower the cerebrospinal fluid pressure in the lumbar cistern of patients who already have imaging evidence of a shift of brain tissue into neighboring compartments. The laws of physics dictate that when a pressure gradient develops between two compartments, there will be a movement to equilibrate this difference. When this occurs rapidly across the foramen magnum and without ample and free-flowing intracranial cerebrospinal fluid in reserve, brain tissue will shift. This produces neurologic impairment which may progress to stupor or coma if untreated. However, many patients with intracranial lesions with favorable characteristics can safely receive neuraxial anesthetics, as is catalogued in the online supplementary material to our review.1
We thank Dr. Derakhshan for reinforcing the point that that not all patients with intracranial lesions will develop devastating neurologic complications from brain herniation, and hope that our article has empowered the reader to be a more thoughtful participant in the conversation about what anesthesia technique is best for individual patients.
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Competing Interests

The authors declare no competing interests.
Lisa R. Leffert, M.D., Lee H. Schwamm, M.D.
Massachusetts General Hospital, Boston, Massachusetts (L.R.L.). lleffert@partners.org
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References

1. Leffert LR, Schwamm LH. Neuraxial anesthesia in parturients with intracranial pathology: A comprehensive review and reassessment of risk. ANESTHESIOLOGY. 2013;119:703–18

2. Maramattom BV, Wijdicks EF. Uncal herniation. Arch Neurol. 2005;62:1932–5

3. Pearce JMS. Kernohan’s notch. Eur Neurol. 2006;55:230–2

4. Larner AJ. False localising signs. J Neurol Neurosurg Psychiatry. 2003;74:415–8

5. McKenna C, Fellus J, Barrett AM. False localizing signs in traumatic brain injury. Brain Inj. 2009;23:597–601

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