primary goals of stroke
management are to reduce brain injury and promote maximum
patient recovery. Rapid detection and appropriate emergency
medical care are essential for optimizing health outcomes.
When available, patients are admitted to an acute stroke
unit for treatment. These units specialize in providing
medical and surgical care aimed at stabilizing the patient’s
Standardized assessments are also performed to aid in the
development of an appropriate care plan.
Current research suggests that stroke units may be effective
in reducing in-hospital fatality rates and the length of
a patient is medically stable, the focus of their recovery
shifts to rehabilitation. Some patients are transferred
to in-patient rehabilitation programs, while others may
be referred to out-patient services or home-based care.
In-patient programs are usually facilitated by an interdisciplinary
team that may include a physician, nurse, physical
and language pathologist, psychologist,
and recreation therapist.
The patient and their family/caregivers also play an integral
role on this team. The primary goals of this sub-acute phase
of recovery include preventing secondary health complications,
minimizing impairments, and achieving functional goals that
promote independence in activities
of daily living.
the later phases of stroke recovery, patients are
encouraged to participate in secondary prevention programs
for stroke. Follow-up is usually facilitated by the patient’s
primary care provider.
initial severity of impairments and individual characteristics,
such as motivation, social support, and learning ability,
are key predictors of stroke recovery outcomes.
Responses to treatment and overall recovery of function
are highly dependent on the individual. Current evidence
indicates that most significant recovery gains will occur
within the first 12 weeks following a stroke.
of stroke neuro-rehabilitation
1620, Johan Wepfer, by studying the brain of a pig, developed
the theory that stroke was caused by an interruption of
the flow of blood to the brain.
After that, the focus became how to treat patients with
most of the last century, people were discouraged from being
active after a stroke. Around the 1950s, this attitude changed,
and health professionals began prescription of therapeutic
exercises for stroke patient with good results. At that
point, a good outcome was considered to be achieving a level
of independence in which patients are able to transfer from
the bed to the wheelchair without assistance.
the early 1950s, Twitchell began studying the pattern of
recovery in stroke patients. He reported on 121 patients
whom he had observed. He found that by four weeks, if there
is some recovery of hand function, there is a 70% chance
of making a full or good recovery. He reported that most
recovery happens in the first three months, and only minor
recovery occurs after six months.
More recent research has demonstrated that significant improvement
can be made years after the stroke.
the same time, Brunnstrom also described the process of
recovery, and divided the process into seven stages. As
knowledge of the science of brain recovery improved, intervention
strategies have evolved. Knowledge of strokes and the process
of recovery after strokes has developed significantly in
the late 20th century and early 21st century.
perspectives and therapeutic avenues
Rehabilitation by Carlo Perfetti concept", widespread
in many countries, is an original motor re-learning theories
idea for constraint-induced therapy is at least 100 years
old. Significant research was carried out by Robert Oden.
He was able to simulate a stroke in a monkey's brain, causing
He then bound up the monkey's good arm, and forced the monkey
to use his bad arm, and observed what happened. After two
weeks of this therapy, the monkeys were able to use their
once hemiplegic arms again. This is due to neuroplasticity.
He did the same experiment without binding the arms, and
waited six months past their injury. The monkeys without
the intervention were not able to use the affected arm even
six months later. In 1918, this study was published, but
it received little attention.
researchers began to apply his technique to stroke patients,
and it came to be called constraint-induced
movement therapy. Notably, the initial studies focused
on chronic stroke patients who were more than 12 months
past their stroke. This challenged the belief held at that
time that no recovery would occur after one year. The therapy
entails wearing a soft mitt on the good hand for 90% of
the waking hours, forcing use of the affected hand. The
patients undergo intense one-on-one therapy for six to eight
hours per day for two weeks.
that supports the use of constraint induced movement therapy
has been growing since its introduction as an alternative
treatment method for upper limb motor deficits found in
Recently, constraint induced movement therapy has been shown
to be an effective rehabilitation technique at varying stages
of stroke recovery to improve upper limb motor function
and use during daily activities of living. The greatest
gains are seen among persons with stroke who exhibit some
wrist and finger extension in the effected limb.
Transcranial magnetic stimulation and brain imaging studies
have demonstrated that the brain undergoes plastic changes
in function and structure in patients that perform constraint
induced movement therapy. These changes accompany the gains
in motor function of the paretic upper limb. However, there
is no established causal link between observed changes in
brain function/structure and the motor gains due to constraint
induced movement therapy.
practice of movements, has been shown in many studies
to be effective in promoting recovery of both arm and leg
function after a stroke.
It is often used by physical or occupational therapists
in the rehab or homehealth setting, but can also be used
as part of a patient's independent home exercise program.
Mental Movement Therapy is one product available for assisting
patients with guided mental imagery.
work represents a paradigm shift in the approach towards
rehabilitation of the stroke-injured brain away from pharmacologic
flooding of neuronal receptors and instead, towards targeted
In layman's terms, this electrical stimulation mimics the
action of healthy muscle to improve function and aid in
retraining weak muscles and normal movement. Functional
Electrical Stimulation (FES) is commonly used in ‘foot-drop’
following stroke, but it can be used to help retrain movement
in the arms or legs.
patients undergoing rehabilitation with a stroke population
or other central nervous system disorders (cerebral palsy,etc.),
also known as Neurodevelopmental
Treatment (NDT), is often the treatment of choice in
North America. The Bobath concept is best viewed as a framework
for interpretation and problem solving of the individual
patient’s presentation, along with their potential for improvement.
Components of motor control that are specifically emphasized,
are the integration of postural control and task performance,
the control of selective movement for the production of
coordinated sequences of movement and the contribution of
sensory inputs to motor control and motor learning.
Task practice is a component of a broad approach to treatment
that includes in-depth assessment of the movement strategies
utilized by the patient to perform tasks, and identification
of specific deficits of neurological and neuromuscular functions.
Many studies have been conducted comparing NDT with other
treatment techniques such as proprioceptive
neuromuscular facilitation (PNF stretching), as well
as conventional treatment approaches (utilizing traditional
exercises and functional activities), etc.
Despite being widely used, based on the literature, NDT
has failed to demonstrate any superiority over other treatment
In fact, the techniques compared with NDT in these studies
often produce similar results in terms of treatment effectiveness.
Research has demonstrated significant findings for all these
treatment approaches when compared with control subjects
and indicate that overall, rehabilitation is effective.
It is important to note, however, that the NDT philosophy
of “do what works best” has led to heterogeneity in the
literature in terms of what constitutes an NDT technique,
thus making it difficult to directly compare to other techniques.
therapy (MT) has been employed with some success in
treating stroke patients. Clinical studies that have combined
mirror therapy with conventional rehabilitation have achieved
the most positive outcomes.
However, there is no clear consensus as to its effectiveness.
In a recent survey of the published research, Rothgangel
stroke patients, we found a moderate quality of evidence
that MT as an additional therapy improves recovery of
arm function after stroke. The quality of evidence regarding
the effects of MT on the recovery of lower limb functions
is still low, with only one study reporting effects. In
patients with CRPS and PLP, the quality of evidence is
cells therapies (in research)
of bone-marrow derived mesenchymal stem cells (MSCs) in
the treatment of ischemic stroke
terminal differentiation of some somatic
stem cells has recently been called into question
after studies of transplanted haematopoietic stem cells
showed the development of myoblasts,
and neuroectodermal cells,
suggesting pluripotency. These findings have led to MSCs
being considered for treatment of ischemic stroke,
specifically in directly enhancing neuroprotection and the
neurorestorative processes of neurogenesis,
mechanisms of neurorestoration and neuroprotection by MSCs
of MSCs into excitable neuron-like cells has been shown
to be possible in
and these cells respond to common central nervous system
However, it is unlikely that this degree of transdifferentiation
occurs in vivo
and that <1% of injected MSCs become truly differentiated
and integrate in the damaged area.
This suggests that transdifferentiation of MSCs into neurons
or neuron-like cells is not a major mechanism by which MSCs
(development of new neurons) is another possible mechanism
of neurorestoration; however its correlation with functional
improvement after stroke is not well established.
The inducted cells likely originate from the ventricular
zone, subventricular zone and choroid plexus, and migrate
to the areas in their respective hemispheres which are damaged.
Unlike the induction of neurogenesis, the induction of angiogenesis
(development of new blood vessels) by MSCs has been associated
with improvements in brain function after ischemic strokes
and is linked to improved neuronal recruitment.
In addition, synaptogenesis
(formation of new synapses between neurons) has been shown
to increase after MSC treatment;
this combination of improved neurogenesis, angiogenesis
and synaptogenesis may lead to a more significant functional
improvement in damaged areas as a result of MSC treatment.
treatment also has shown to have various neuroprotective
including reductions in apoptosis,
inflammation and demyelination, as well as increased astrocyte
MSC treatment also appears to improve the control of cerebral
blood flow and blood–brain barrier permeability,
as well as what is currently thought to be the most important
mechanism of MSC treatment after stroke, the activation
of endogenous neuroprotection and neurorestoration pathways
by the release of cytokines and trophic factors.
activation of endogenous neuroprotection and neurorestoration
probably has a major part in the improvement of brain function
after stroke, it is likely that the functional improvements
as a result of MSC treatment are due to combined action
via multiple cellular and molecular mechanisms to affect
neurorestoration and neuroprotection, rather than just a
single mechanism. These effects are also modulated by key
variables, including the number of and type of MSCs used,
timing of treatment relative to when the patient’s stroke
occurred, route of delivery of the MSCs, as well as patient
variables (e.g. age, underlying conditions).
this means for stroke patients and the limitations or concerns
with MSCs as a potential treatment
MSC treatment becomes available for stroke patients, it
is possible that current mortality and morbidity rates could
substantially improve due to the direct enhancement of neuroprotection
and neurorestoration mechanisms rather than only indirect
facilitation or prevention of further damage, e.g. decompressive
surgery. However, for MSC treatment to be used effectively
and safely in a clinical setting, more research needs to
be conducted, specifically in the areas of determining the
relative influences of key variables (especially patient
variables) on patient outcomes as well quantifying potential
risks, e.g. tumour formation. Although ethical concerns
are mostly limited to the use of embryonic
it may also be important to address any possible ethical
concerns (however unlikely) over the use of somatic stem
of muscles affected by the Upper Motor Neuron Syndrome
affected by the Upper Motor Neuron Syndrome have many potential
features of altered performance including: weakness, decreased
motor control, clonus (a series of involuntary rapid muscle
contractions), exaggerated deep tendon reflexes, spasticity
and decreased endurance. The term "spasticity" is often
erroneously used interchangeably with Upper Motor Neuron
Syndrome, and it is not unusual to see patients labeled
as spastic who demonstrate an array of UMN findings.
has been estimated that approximately 65% of individuals
develop spasticity following stroke,
and studies have revealed that approximately 40% of stroke
victims may still have spasticity at 12 months post-stroke.
The changes in muscle tone probably result from alterations
in the balance of inputs from reticulospinal and other descending
pathways to the motor and interneuronal circuits of the
spinal cord, and the absence of an intact corticospinal
In other words, there is damage to the part of the brain
or spinal cord that controls voluntary movement.
means are available for the treatment of the effects of
the Upper Motor Neuron Syndrome. These include: exercises
to improve strength, control and endurance, nonpharmacologic
therapies, oral drug therapy, intrathecal drug therapy,
injections, and surgery.
While Landau suggests that researchers do not believe that
treating spasticity is worthwhile, many scholars and clinicians
continue to attempt to manage/treat it.
group of researchers concluded that while spasticity may
contribute to significant motor and activity impairments
post-stroke, the role of spasticity has been overemphasized
in stroke rehabilitation.
In a survey done by the National Stroke Association, while
58 percent of survivors in the survey experienced spasticity,
only 51 percent of those had received treatment for the
should be based on assessment by the relevant health professionals.
For muscles with mild-to-moderate impairment, exercise
should be the mainstay of management, and is likely to need
to be prescribed by a physiotherapist.
with severe impairment are likely to be more limited in
their ability to exercise and may require help to do this.
They may require additional interventions, to manage the
greater neurological impairment and also the greater secondary
complications. These interventions may include serial casting,
flexibility exercise such as sustained positioning programs,
and patients may require equipment, such as using a standing
frame to sustain a standing position. Applying specially
made Lycra garments may also be beneficial.
is beneficial in this area as it helps post-stroke
individuals to progress through the stages of motor recovery.
These stages were originally described by Twitchell and
Brunnstrom, and may be known as the Brunnstrom
Initially, post-stroke individuals suffer from flaccid paralysis.
As recovery begins, and progresses, basic movement synergies
will develop into more complex and difficult movement combinations.
may develop and become quite severe before it begins to
decline (if it does at all).
Although an overall pattern of motor recovery exists, there
is much variability between each individual’s recovery.
As previously described, the role of spasticity in stroke
is controversial. However, physiotherapy can help to improve
motor performance, in part, through the management of spasticity.
will result in the maintenance of abnormal resting limb
postures which can lead to contracture
In the arm, this may interfere with hand
hygiene and dressing, whereas in the leg, abnormal resting
postures may result in difficulty transferring. In order
to help manage spasticity, physiotherapy
interventions should focus on modifying or reducing muscle
Strategies include mobilizations of the affected limbs early
along with elongation of the spastic muscle and sustained
In addition, the passive manual technique of rhythmic rotation
can help to increase initial range.
Activating the antagonist
(muscle) in a slow and controlled movement is a beneficial
training strategy that can be used by post-stroke individuals.
Splinting, to maintain muscle stretch and provide tone inhibition,
and cold (i.e. in the form of ice packs), to decrease neural
firing, are other strategies that can be used to temporarily
decrease the extent of spasticity.
The focus of physiotherapy for post-stroke individuals is
to improve motor performance, in part, through the manipulation
of muscle tone.
medications used for the treatment of spasticity include:
and even cannabinoid-like
compounds.³ The exact mechanism of these medications is
not fully understood, but they are thought to act on neurotransmitters
or neuromodulators within the central nervous system (CNS)
or muscle itself, or to decrease the stretch reflexes. The
problem with these medications is their potential side effects
and the fact that, other than lessening painful or disruptive
spasms and dystonic postures, drugs in general have not
been shown to decrease impairments or lessen disabilities.
administration of drugs involves the implantation of a pump
that delivers medication directly to the CNS.
The benefit of this is that the drug remains in the spinal
cord, without traveling in the bloodstream, and there are
often fewer side effects. The most commonly used medication
for this is baclofen
sulfate and Fentanyl
have been used as well, mainly for severe pain as a result
of the spasticity.
are focal treatments administered directly into the spastic
muscle. Drugs used include: Botulinum
toxin (BTX), phenol,
alcohol, and lidocaine.
Phenol and alcohol cause local muscle damage by denaturing
protein, and thus relaxing the muscle. Botulinum toxin is
and it relaxes the muscle by preventing the release of a
Many studies have shown the benefits of BTX
and it has also been demonstrated that repeat injections
of BTX show unchanged effectiveness.
treatment for spasticity includes lengthening or releasing
of muscle and tendons, procedures involving bones, and also
selective dorsal rhizotomy.
Rhizotomy, usually reserved for severe spasticity, involves
cutting selective sensory nerve
roots, as they probably play a role in generating spasticity.
subluxation following stroke
(or shoulder) subluxation
is defined as a partial or incomplete dislocation
of the shoulder joint that typically results from changes
in the mechanical integrity of the joint. Subluxation is
a common problem with hemiplegia,
or weakness of the musculature of the upper limb. Traditionally
this has been thought to be a significant cause of post-stroke
shoulder pain, although a few recent studies have failed
to show a direct correlation between shoulder subluxation
exact etiology of subluxation in post-stroke patients is
unclear but appears to be caused by weakness of the musculature
supporting the shoulder joint. The shoulder is one of the
most mobile joints in the body. To provide a high level
of mobility the shoulder sacrifices ligamentous stability
and as a result relies on the surrounding musculature (i.e.,
cuff muscles, latissimus
dorsi, and deltoid)
for much of its support. This is in contrast to other less
mobile joints such as the knee and hip, which have a significant
amount of support from the joint capsule and surrounding
ligaments. If a stroke damages the upper motor neurons controlling
muscles of the upper limb, weakness and paralysis, followed
by spasticity occurs in a somewhat predictable pattern.
The muscles supporting the shoulder joint, particularly
and posterior deltoid become flaccid and can no longer offer
adequate support leading to a downward and outward movement
of arm at the shoulder joint causing tension on the relatively
capsule. Other factors have also been cited as contributing
to subluxation such as pulling on the hemiplegic arm and
can usually be made by palpation
or by feeling the joint and surrounding tissues, although
there is controversy as to whether or not the degree of
subluxation can be measured clinically. If shoulder subluxation
occurs, it can become a barrier to the rehabilitation process.
Treatment involves measures to support the subluxed joint
such as taping the joint, using a lapboard
or armboard. A shoulder sling may be used, but is controversial
and a few studies have shown no appreciable difference in
range-of-motion, degree of subluxation, or pain when using
a sling. A sling may also contribute to contractures and
increased flexor tone if used for extended periods of time
as it places the arm close to the body in adduction,
rotation and elbow flexion.
Use of a sling can also contribute to learned nonuse by
preventing the functional and spontaneous use of the affected
upper extremity. That said, a sling may be necessary for
some therapy activities. Slings may be considered appropriate
during therapy for initial transfer and gait
training, but overall use should be limited. As the
patient begins to recover, spasticity
and voluntary movement of the shoulder will occur as well
as reduction in the shoulder subluxation. Slings are of
no value at this point.
electrical stimulation (FES) has also shown promising
results in treatment of subluxation, and reduction of pain,
although some studies have shown a return of pain after
discontinuation of FES. More recent research has failed
to show any reduction of pain with the use of FES.
treatment consists of preventive measures such as early
of motion, proper positioning, passive support of soft
tissue structures and possibly early re-activation of
shoulder musculature using functional electrical stimulation.
Aggressive exercises such as overhead pulleys should be
avoided with this population.
Teasell RW: "The Painful Hemiplegic Shoulder". Physical
Medicine and Rehabilitation: State of the Art Reviews 1998;
12 (3): 489-500.
2. Boyd EA, Goudreau L, O'Riain MD, et al.: A radiological
measure of shoulder subluxation in hemiplegia: its reliability
and validity. Arch Phys Med Rehabil 1993 Feb; 74(2): 188-93
3. Brandstater ME: Stroke rehabilitation. In: DeLisa JA,
et al., eds. Rehabilitation Medicine: Principles and Practice.
3rd ed. Philadelphia: Lippincott-Raven;
4. Chae J, Yu DT, Walker ME, et al.: Intramuscular electrical
stimulation for hemiplegic shoulder pain: a 12-month follow-up
of a multiple-center, randomized clinical trial. Am J Phys
Med Rehabil. 2005 Nov; 84(11): 832-42
5. Chantraine A, Baribeault A, Uebelhart D, Gremion G: Shoulder
pain and dysfunction in hemiplegia: effects of functional
electrical stimulation. Arch Phys Med Rehabil 1999 Mar;
Post-stroke Pain (CPSP) is neuropathic pain which is caused
by damage to the neurons in the brain (central nervous system),
as the result of a vascular injury. One study found that
up to 8% of people who have had a stroke will develop Central
Post-stroke Pain, and that the pain will be moderate to
severe in 5% of those affected.
The condition was formerly called “thalamic
pain”, because of the high incidence among those with
damage to the thalamus
nuclei. Now known as CPSP, it is characterized by perceived
pain from non-painful stimuli, such as temperature and light
touch. This altered perception of stimuli, or allodynia,
can be difficult to assess due to the fact that the pain
can change daily in description and location, and can appear
anywhere from months to years after the stroke. CPSP can
also lead to a heightened central response to painful sensations,
Affected persons may describe the pain as cramping,
burning, crushing, shooting, pins
and needles, and even bloating
Both the variation and mechanism of pain in CPSP have made
it difficult to treat. Several strategies have been employed
by physicians, including intravenous lidocaine, opioids/narcotics,
medications and neurosurgical
procedures with varying success. Higher rates of successful
pain control in persons with CPSP can be achieved by treating
other sequelae of stroke, such as depression and spasticity.
As the age of the population increases, the diagnosis and
management of CPSP will become increasingly important to
improve the quality of life of an increasing number of stroke
uncommon, less understood result of stroke is a condition
This condition was initially recognized as: ‘Disorders of
the execution of learned movements which cannot be accounted
for by either weakness, incoordination, or sensory loss,
nor by incomprehension of, or inattention to commands.’
Several forms of apraxia are recognized.
Limb-kinetic apraxia is the inability to make precise or
exact movements with a finger, an arm or a leg. idiomotor
apraxia is the inability to carry out a command from the
brain to mimic limb or head movements performed or suggested
by others. Conceptual apraxia is similar to idiomotor apraxia,
but infers a more profound malfunctioning in which the function
of tools or objects is no longer understood. Ideational
apraxia is the inability to create a plan for a specific
movement. Buccofacial apraxia, or facial-oral apraxia, is
the inability to coordinate and carry out facial and lip
movements such as whistling, winking, coughing, etc. on
command. Constructional apraxia affects the person’s ability
to draw or copy simple diagrams, or to construct simple
figures. Oculomotor apraxia is a condition in which the
patient finds it difficult to move his/her eyes. Many believe
that the most common form of apraxia is ideamotor apraxia,
in which a disconnection between the area of the brain containing
plans for a movement and the area of the brain that is responsible
for executing that movement occurs.
many effects of stroke, where the clinician is able to judge
the particular area of the brain that a stroke has injured
by certain signs or symptoms, the causation of apraxia is
less clear. A common theory is that the part of the brain
that contains information for previously learned skilled
motor activities has been either lost or cannot be accessed.
The condition is usually due to an insult to the dominant
hemisphere of the brain. More often this is located in the
frontal lobe of the left hemisphere of the brain. Treatment
of acquired apraxia due to stroke usually consists of physical,
occupational, and speech therapy. The Copenhagen Stroke
Study, which is a large important study published in 2001,
showed that out of 618 stroke patients, manual apraxia was
found in 7% and oral apraxia was found in 6%.
Both manual and oral apraxia were related to increasing
severity of stroke. Oral apraxia was related with an increase
in age at the time of the stroke. There was no difference
in incidence among gender. It was also found that the finding
of apraxia has no negative influence on ability to function
after rehabilitation is completed. The National Institute
of Neurological Disorders and Stroke (NINDS) is currently
sponsoring a clinical trial to gain an understanding of
how the brain operates while carrying out and controlling
voluntary motor movements in normal subjects. The objective
is to determine what goes wrong with these processes in
the course of acquired apraxia due to stroke or brain injury.
medullary syndrome, also known as Wallenberg’s Syndrome,
is caused by blockage of the posterior
inferior cerebellar artery (PICA) or the vertebral
arteries. Signs and symptoms include decreased pain
and temperature on the same side of the face and opposite
side of the body compared to the lesion, ataxia
on the same side of the lesion, and Horner's
syndrome on the same side of the face.
in the acute setting is mostly focused on symptomatic management.
After initial treatment in the hospital, some patients will
need short-term placement in a nursing home or rehabilitation
facility before going home. Rehabilitation in Wallenberg’s
Syndrome focuses on improving balance, coordination, working
on activities of daily living, and improving speech and
swallowing function. Severe nausea
can be present and limit progress in rehabilitation and
recovery. Symptomatic treatment with anti-emetics
and medications for the hiccups are important. Commonly
used anti-emetics include odansetron,
These medications are also used to treat hiccups,
along with chlorpromazine.
There are case reports of other medications useful in treating
hiccups in Wallenberg’s Syndrome including baclofen
medications. The prognosis for someone with lateral
medullary syndrome depends upon the size and location of
damaged area of the brain stem. Some individuals recover
quickly while others may have significant neurological disabilities
for months to years after the initial injury.
Hiccups Associated with Lateral Medullary Syndrome: A Case
Report. American Journal of Physical Medicine & Rehabilitation.
76(2):144-146, March/April 1997. Nickerson, Robert B. MD
2; Atchison, James W. DO 3; Van Hoose, James D. MD; Hayes,
2. Physical Medicine and Rehabilitation Board Review (Paperback).
Sara J. Cuccurullo
4. Dysphagia in Lateral Medullary Infarction (Wallenberg’s
Syndrome) . An Acute Disconnection Syndrome in Premotor
Neurons Related to Swallowing Activity? Stroke. 2001;32:2081.
Ibrahim Aydogdu, MD; Cumhur Ertekin, MD; Sultan Tarlaci,
MD; Bulent Turman, MD, PhD; Nefati Kiylioglu, MD Yaprak
is a commonly reported consequence of stroke and is seen
in anywhere from 25-50% of patients. The Diagnostic
and Statistical Manual (DSM-IV-TR) defines post-stroke
depression as “a mood disorder due to a general medical
condition (i.e. stroke) that is judged to be due to the
direct physiological effects of [that] condition.” Post-stroke
depression may involve depressed mood and decreased interest
and pleasure that impairs social and occupational functioning,
but does not necessarily need to meet the full criteria
of a major depressive disorder.
first studies to look for an association between specific
stroke lesions and the occurrence of depression reported
a correlation between left frontal lesions and major depression.
Damage to the frontal noradrenergic,
projections were thought to cause a depletion of catecholamines,
leading to depression. However, more recent studies have
demonstrated that the anatomic aspects of a lesion do not
necessarily correlate with the occurrence of depression.
Other psychological factors can lead to the development
of depression including personal and social losses related
to the physical disabilities often caused by a stroke.
incidence of post-stroke depression peaks at 3–6 months
and usually resolves within 1–2 years after the stroke,
although a minority of patients can go on to develop chronic
depression. The diagnosis of post-stroke depression is complicated
by other consequences of stroke such as fatigue
retardation – which do not necessarily indicate the
presence of depression. Loss of interest in activities and
relationships should prompt an evaluation for depression.
antidepressants (TCAs), such as nortriptyline,
have been used in the treatment of post-stroke depression.
More recently, the selective
serotonin reuptake inhibitors (SSRIs), such as fluoxetine
have become the pharmacologic therapy of choice due to the
lower incidence of side
effects. Also, psychologic treatment such as cognitive
behavioral therapy, group
therapy, and family
therapy are reported to be useful adjuncts to treatment.
the development of post-stroke depression can play a significant
role in a patient’s recovery from a stroke. For instance,
the severity of post-stroke depression has been associated
with severity of impairment in activities
of daily living (ADLs). By effectively treating depression,
patients experience a greater recovery of basic ADLs such
as dressing, eating and ambulating, as well as instrumental
ADLs, such as the ability to take care of financial and
household matters. In essence, recognition and treatment
of post-stroke depression leads to greater functional ability
for the patient over time.