Second edition

11.qxd 3/10/08 9:49 AM Page 457
Figure 11.2 Note the wide cavum septi pellucidi in the brain of
a professional boxer. (Reproduced from Graham and Lantos 1996.)
had a traumatic subarachnoid hemorrhage followed by the
gradual development of a communicating hydrocephalus.
Clinically, although perhaps having a ‘magnetic’ gait, such
patients do not develop parkinsonism; furthermore, on
imaging, the ventricular dilation will be out of all proportion
to any cortical atrophy. Chronic subdural hematoma must
also be considered but is readily diagnosed on imaging.
Treatment
The general treatment of dementia is discussed in Section
5.1. In cases in which parkinsonism is prominent, consideration
may be given to a trial of levodopa.
11.4 POST-CONCUSSION SYNDROME
Concussion is characterized by a brief loss of consciousness
or merely a sense of being dazed, occurring immediately
after a blow to the head or, in some cases, a whiplash injury
(Miller 1982); patients also experience a variable, but
short, period of amnesia, with both retrograde and anterograde
components. Most recover fairly promptly, however,
in a minority a post-concussion syndrome will develop.
Post-concussion syndrome, also known as post-concussional
disorder, is characterized by headache, difficulty with concentration
and memory, fatigue, dizziness, various admixtures
of depression, irritability and anxiety, and other
symptoms, such as photophobia.
Clinical features
As noted, concussion may be associated with a loss of consciousness
and this generally lasts only a minute or so; in
11.4 Post-concussion syndrome 457
other cases, patients may remain conscious but appear
‘dazed’ and mildly confused, with these symptoms again
resolving quickly. The amnesia seen in concussion extends in
a retrograde fashion for up to hours and in an anterograde
fashion from minutes to, in rare cases, hours (Fisher 1966;
Martland 1928). In a very small minority of cases, concussion
may be associated with a grand mal seizure occurring
within seconds of the impact; also known as ‘concussive
convulsions’, these events do not recur and do not portend
the development of epilepsy (McCrory et al. 1997).
Although the grosser aspects of concussion clear immediately,
there may be some subtle and mild difficulty with
memory and concentration that typically resolves gradually
within a week (McCrea et al. 2003); in those with a history
of prior concussion, however, these symptoms may
take longer to resolve (Guskiewicz et al. 2003).
In a minority of cases, concussion may be followed by
the post-concussion syndrome (Lishman 1968; Mapothar
1937; Symonds 1962). In these cases, in addition to the
cognitive difficulties just described, other symptoms
become evident within the first day and then persist.
Headache tends to be severe and may be continuous or
episodic; it may be dull and continuous, or throbbing, and
may be exacerbated by loud noises, coughing or sneezing.
Fatigue may be constant or may become evident only when
patients exert themselves. Dizziness may consist of mere
light-headedness or there may be a true vertigo; when vertigo
is present, patients may complain that it is exacerbated
or precipitated by changes in position or by any sudden
movements. Depression may occur and may be marked by
severe insomnia. Irritability may be prominent, and
patients may complain of great difficulty controlling their
tempers. Anxiety may also be seen but appears less common.
Other symptoms may occur, including photophobia,
hyperacusis, and hyperhidrosis, which at times may be
quite impressive. Many patients report that alcohol exacerbates
their symptoms.
Course
In most cases, a gradual remission of symptoms occurs
anywhere from a few weeks up to 3 years after the concussion,
with the majority of patients recovering in a matter of
months. When symptoms persist for more than 3 years, a
chronic, indefinite, course may be anticipated.
Etiology
Although concussion probably occurs secondary to a fully
reversible disruption of axonal function, the post-concussion
syndrome in all likelihood occurs secondary to a mild
degree of diffuse axonal injury, as indicated by MR scanning
(Hofman et al. 2001) and in one autopsy case of a
patient with the syndrome who died 7 months after the
concussion of an unrelated cause (Bigler 2004).