Review Article

Systemic use of corticosteroids

in neurological disorders
Miguel D’haeseleer1,2
1
Universitair Ziekenhuis Brussel, Vrije Universiteit Brussel, Brussels, 2National Multiple Sclerosis Center,
Melsbroek, Belgium

Abstract
Corticosteroids have been used for almost 60 years in medicine and their roles in patients have
always been discussed by researchers and clinicians dedicated in the related field. Now they
are still used in treatment of patients with neurological disorders. Usually Corticosteroids are
used to decrease inflammations. In this review, we present five key indications, i.e., bacterial
meningitis, myasthenia gravis, Bell’s palsy and giant cell (temporal) arteritis for the systemic
use of corticosteroids in neurology based on a mix of prevalence, quality of evidence and
impact on disease management.

Key words: corticosteroids, systemic use, neurological disorders, prednisone

INTRODUCTION Corticosteroids are used in the treatment

Address for Correspondence:
Dr. Miguel D’haeseleer,
Universitair Ziekenhuis Brussel, Vrije
Universiteit Brussel, Brussels, National
Multiple Sclerosis Center, Melsbroek,
Belgium.
E-mail: Miguel.DHaeseleer@uzbrussel.be
Access this article online
Website:
www.intern-med.com
DOI:
10.4103/2224-4018.135603
Quick Response Code:
Corticosteroids were introduced in medicine
almost 60 years ago and are still used in an
exhaustive list of neurological disorders.
In some conditions, their use is supported
by solid scientific data obtained from
randomized controlled trials, systematic
reviews and/or meta-analyses. Other
indications, however, depend largely on
clinical experience and expert opinion. In
this paper, we present five key indications
for the use of systemic cort icosteroids in the
field of neurology. Our selection was based
on a mix of prevalence, quality of evidence
and impact on disease management.
MULTIPLE SCLEROSIS
Multiple sclerosis (MS) is a major cause of
neurological disability in young adults.[1] The
exact cause is unknown. Most patient start
with a relapsing-remitting disease course,
but there is also a secondary or primary
progressive stage. Pathologically, focal
inflammatory lesions with demyelination
in the central nervous system form the
substrate of typical white matter lesions
and clinical relapses. Progressive and global
axonal degeneration is considered as the
main determinant of long-term disability.[2]
of MS relapses with disabling symptoms
(e.g., limb weakness, vision loss, cerebellar
dysfunction, pain, etc.). Intravenous (IV)
methylprednisolone 1 g daily for 5 days is
a common regimen. A Cochrane review
published in 2000 showed significant
improvement with corticosteroids versus
placebo in patients when evaluated after
5 weeks. Longer-duration protocols did
not lead to better results. Only one study
examined the neurological outcome after >1
year of follow-up and found no significant
difference between treatment groups.[3]
These results suggest that corticosteroids
hasten recuperation in disabling MS relapses,
but the long-term outcome remains unsure.
Orally administered methylprednisolone is
probably equally effective to IV, but there
may be higher risk of side-effects and
recurrent optic neuritis.[4,5]
There is no solid evidence for the chronic
use of glucocorticoids as disease-modifying
treatment in relapsing-remitting or
progressive MS.
BACTERIAL MENINGITIS
Streptococcus pneumoniae and Neisseria
meningitidis are important causes of bacterial
meningitis in immunocompetent adults.

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 D’haeseleer: Corticosteroids in neurological disorders
Classic bacterial meningitis still has substantial mortality
and morbidity. Possible complications include septic
shock, disseminated intravascular coagulation, arthritis,
hearing loss or other cranial nerve problems, epilepsy,
hydrocephalus, and intracranial thrombosis.
Possible benefit of adjuvant treatment with corticosteroids
was first suggested by following observations in animals
studies: Hearing loss correlated with the amount
of inflammation in the cerebrospinal fluid (CSF); [6]
dexamethasone reduced the level of inflammatory cytokines
in the CSF.[7] Corticosteroids should be administered prior
to or together with the first dose of antibiotics, because at
that point the bulk of inflammation-triggering intracellular
antigens is expected to be released.
Results of clinical studies in humans are conflicting. The
2002 European Dexamethasone Study evaluated the effect
of dexamethasone versus placebo in 301 patients with
bacterial meningitis. Mortality and neurological outcome
were significantly better with corticosteroids at 8 weeks
in patients with pneumococcal meningitis.[8] In contrast,
studies in Malawi and Vietnam showed no benefit of
treatment with dexamethasone.[9,10] Recently, a Cochrane
meta-analysis examined over 4000 patients with bacterial
meningitis worldwide. Treatment with corticosteroids did
not change overall mortality, but survival was significantly
better in patients with pneumococcal meningitis.
Dexamethasone reduced rates of hearing loss and short-
term neurological dysfunction in high-income countries,
while this was not the case in low-income countries.[11]
Based on the available evidence, early administration
of dexamethasone 10 mg IV every 6 h for 4 days, or
until CSF cultures reveal a nonpneumococcal pathogen,
is recommended for adults suspected with bacterial
meningitis in developed regions.
MYASTHENIA GRAVIS
Myasthenia gravis (MG) is pathology of neuromuscular
transmission caused by an autoimmune response against
the postsynaptic membrane. Most patients have serum
antibodies against the nicotinic acetylcholine receptor.
Clinical features include skeletal muscle weakness and
fatigability.
More severe forms generally respond well to with high-
dose oral prednisone (1 mg/kg daily). Evidence is based on
observational studies.[12,13] It is usually advised to start this
regime in hospital-setting because some patients develop
a transient worsening of MG symptoms (after 5-10 days),
which may lead to respiratory insufficiency. [13,14] An
escalation regimen starting at a lower dose (e.g., 20 mg/day)
can avoid this risk in ambulatory patients.[15]
JOURNAL OF TRANSLATIONAL INTERNAL MEDICINE / APR-JUN 2014 / VOL 2 | ISSUE 2
BELL’S PALSY
Bell’s palsy is an acute peripheral facial nerve palsy
of unknown etiology. Inflammation and compression
within the canalis facialis of the petrous bone may play
a role in the pathophysiology. Patients typically present
with unilateral facial paralysis with the inability to close
the eye. Often there also is associated hyperacusis and
decreased taste.
Two recent high-quality randomized controlled trials
have showed that treatment with prednisone, started
within the first 72 h from onset results in faster and better
recovery.[16,17] Prednisone is usually given during 10 days:
60 mg during 5 days and then tapered over 5 days.
GIANT CELL (TEMPORAL) ARTERITIS
Diagnosis of giant cell arteritis (GCA) should be considered
in every elderly patient with new headache complaints,
especially when there are associated manifestations as fever,
weight loss, polymyalgia, jaw claudication, local tenderness/
welling and/or elevated sedimentation rate. The most
feared complication of GCA is visual loss due to anterior
ischemic optic neuropathy.
Early treatment with oral corticosteroids (prednisone
60 mg daily) is recommended, as soon as diagnosis is
suspected. Practice is based on clinical experience, there
are no controlled trials. Patients often show dramatic
response to treatment. If associated visual loss is present,
IV methylprednisolone can be considered during the first
3 days. As in MG, after several weeks of sustained clinical
remission, the dose can be gradually tapered but patients
should be carefully monitored for possible relapses.
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How to cite this article: D’haeseleer M. Systemic use of corticosteroids
in neurological disorders. J Transl Intern Med 2014;2:70-2.
Source of Support: Nil, Conflict of Interest: None declared