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[52]
time to initiate therapy. Studies comparing in-hospital lobe epilepsy (TLE) model, 2 weeks administration of
initiation with outpatient initiation of preventative simvastatin after kainic acid-induced SE lead to not
therapies have consistently shown better compliance only attenuated microscopic morphological changes,
[53]
over the long-term. For stroke patients, participation but also reduced seizure activity in the brain at 4
in a hospital-based prevention initiative with in-hospital to 6-month after SE. On the other hand, 2 weeks
[65]
initiation of antithrombotic, statin and antihypertensive treatment of atorvastatin did not affect the duration of
was associated with very high rates of compliance at 3 SE or development of epilepsy in electrically induced
months. In-hospital initiation of statins is associated rat TLE model. [66]
[54]
with high rates of continuation and achievement of
National Cholesterol Education Program guideline goals. There is no evidence that the neuroprotective properties
[55]
In one study 92 statin-naïve patients with an indication of statin will have a clinical benefit in acute epileptic
for treatment, hospital initiation of statin therapy yielded syndromes.
a 93% rate of adherence, lowered mean low-density
lipoprotein cholesterol levels from 120 to 78 mg/dL CENTRAL NERVOUS SYSTEM INFECTION
and increased the proportion of patients with low-density
lipoprotein cholesterol levels lower than 100 mg from Simvastatin can attenuate leukocyte invasion into the
36% to 88% at 3 months. central nervous system (CNS) and systemic complication
of pneumococcal meningitis in an experimental
[67]
TBI AND SCI model of bacterial meningitis rodents. Simvastatin
treatment significantly reduced cerebrospinal fluid
Statins have demonstrated benefit in animal models of leukocyte counts with dose-dependent manner, but
TBI and spinal cord injury (SCI). Statins treatment prior did not altered cerebellar bacterial titers. The marked
to experimental TBI was associated with reduced the hypothermia was dose-dependently reversed by statin
cortical contusion volume and cerebral edema. [57,58] treatment. This neuroprotective effects can be explained
[56]
Statin therapy after TBI in rat decreased post-traumatic by anti-inflammatory pleiotropic property of the statin.
apoptosis in hippocampus and peri-contusional Statin treatment did not result in an improvement of the
cortex and increased neuronal proliferation leading to clinical score or a reduction of increased intracranial
improvement of cognitive abilities. The experimental pressure and blood-barrier breakdown. Clinical studies
[59]
studies in preclinical SCI models also suggest that statin of the effects of statin treatment in acute CNS infection
treatment could significantly improve functional outcome are lacking.
via anti-inflammatory and anti-apoptotic effects. [60,61]
CONCLUSION
Clinical evidence for the effect of statins moderate to
severe neurotrauma needs further extensive studying. Some preclinical and clinical evidence has shown
Only one small prospective, randomized, double blind that statin therapy following SAH could be safe and
trail of statin treatment initiation within 24 h of moderate beneficial in terms of reducing DCI and possibly
[62]
TBI was found. The study included only 8 patients with cerebral vasospasm and early in-hospital mortality.
statin and the 13 controls. The statin administration was However, methodology of clinical studies was varied
associated with a reduced duration of amnesia (hazard and beneficial effects were inconsistent, statin therapy
ratio 53.76, 95% CI 1.58-1,824.64), but no difference in following SAH should not be considered standard care
disability at 3 months. at this time. Statin use before ICH or before and during
acute ischemic stroke is safe and can reduce in-hospital
STATUS EPILEPTICUS AND EPILEPSY mortality and improve functional outcome, whereas
statin withdrawal in the hospital after acute ischemic
Animal models suggest that statin administration stroke, even for a brief period, can cause early neurologic
might be a therapeutic strategy for epilepsythrough deterioration and death. Despite the lack of clinical
neuroprotection in status epilepticus (SE) and evidence for statin initiation after ICH or acute ischemic
prevention of epileptogenesis progression. [63-66] stroke, we can achieve better long-term compliance with
Lovastatin administration after pilocapine-induced in-hospital initiation when statin therapy is indication.
SE suppressed mRNA expression of hippocampal Even though benefit in preclinical studies, there is no
cytokines (such as interleukin-1b, interleukin-6, tumor clinical evidence that the pleiotropic properties of statins
necrosis factor a, and kinin B1 recepter) and reduced will have a clinical benefit in neurotrauma, epilepsy and
SE-induced hypothermia. Lovastatin also decreased CNS infection.
[63]
cell loss in hippocampal CA1, CA3 and hilus of dentate
gyrus after pilocapine-induced SE that is a critical Financial support and sponsorship
step of epileptogenesis. In the chronic temporal Nil.
[64]

138 Neuroimmunol Neuroinflammation | Volume 3 | June 20, 2016