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ASYMMETRICAL LOWER EXTREMITY POWER DEFICIT AS A RISK FACTOR FOR INJURIOUS FALLS IN HEALTHY OLDER WOMEN
Author(s) -
Portegijs Erja,
Sipilä Sarianna,
Pajala Satu,
Lamb Sarah E.,
Alen Markku,
Kaprio Jaakko,
Koskenvuo Markku,
Rantanen Taina
Publication year - 2006
Publication title -
journal of the american geriatrics society
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.992
H-Index - 232
eISSN - 1532-5415
pISSN - 0002-8614
DOI - 10.1111/j.1532-5415.2006.00643_6.x
Subject(s) - medicine , injury prevention , poison control , physical therapy , occupational safety and health , incidence (geometry) , physical medicine and rehabilitation , emergency medicine , pathology , physics , optics
ours, with a recent history of distant diplopia without headache, although ophthalmological examination did not indicate the existence of papilledema. Cranial nerve VI has the longest intracranial course and is thus vulnerable to variations of the intracranial pressure. It may be damaged between its emergence from the belly of the pons and Dorello’s canal where it enters the cavernous sinus. The association between diplopia and bilateral CSH may correspond to two distinct physiopathological mechanisms. There may be bilateral abducens nerve damage because of the development of intracranial hypertension caused by posttraumatic subdural bleeding. Alternatively, it may be secondary to intracranial hypotension, with downward displacement of the brain, which leads to tearing of dural veins with subsequent subdural bleeding. This could explain the development of diplopia, with a possible secondary subdural hematoma in spontaneous or acquired intracranial hypotension. Nevertheless, the association between bilateral abducens nerve palsy and bilateral CSH is rare. The fact that bilateral CSH is predominantly encountered in older people, whose symptoms in relation to the acute pathology are not always in the foreground and can mislead the clinician, may explain this. The frequency of diplopia may therefore be underestimated. Moreover, CSH is not always correlated with intracranial hypertension. Normal to low pressure rates are reported in 30% to 50% of patients presenting with CSH. The relative slowness of the development of the hematoma, with progressive adaptation of intracranial pressure at the expense of cerebral and liquid compartments, in patients with cerebral atrophy can explain this. This was not the case in our patient, who presented with papilledema related to intracranial hypertension. The hematomas were evacuated under pressure, with a rapid subdural space collapse, which is not the general rule with bilateral CSH. Finally, hypotension was supposed to be the origin of the cranial trauma, and antihypertensive treatment was stopped. This case of bilateral CSH, bilateral VI nerve palsy, and papilledema is rarely mentioned in the literature. Intracranial hypertension was diagnosed with funduscopic examination. Special care must be reported for a thorough history and examination in such patients, often presenting a poor symptomatology that sometimes does not lead directly to the main diagnosis.