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Bio Article & Case
Abstract
I. INTRODUCTION
Stroke is today and will continue to be the most frequent cause of chronic
disability in adults in the western world. Nearly half of the stroke survivors display
neuropsychological deficits acutely after stroke and one in every three stroke patients
is diagnosed with neglect. Although many patients recover from neglect spontaneously
within the first months, ten percent of these individuals still show neglect three months
after right hemisphere cerebral accident. Neglect often predicts a poor functional
outcome.
Neglect has a negative effect on long-term outcome: these patients take longer to
recover and they are left with more functional disabilities than patients with right
hemisphere lesions without neglect. Less than half of neglect patients recover
spontaneously during the first weeks after stroke and less than 10% show complete
recovery. Severe disabilities often lead to lack of co-operation acutely after stroke and
dementia and attention deficits increase the probability of late failure in recovery. Early
admission to rehabilitation decreases long-term adverse outcomes. Hemispatial neglect
and depression are associated with an increased risk of low recovery as assessed in
activities of daily living (ADL), but not on mobility. Previously stroke patients who
improved most at one year follow-up were those with larger lesions and generalized
cognitive impairment at baseline, however, aphasia and neglect were not influencing
the long term recovery.
II. OBJECTIVES
The aim of the present study was to search for the factors associated with
recovery from neglect yet considering the heterogeneity of the syndrome.
III. DESIGN
All 21 patients were followed up at 6 months. The neglect syndrome was assessed
by the conventional subtests of the Behavioural Inattention Test (BIT) and by the
Catherine Bergego Scale (CBS) before and after the 3-week rehabilitation and at 6-
month follow-up.
Year : 2011
Source: http://www.neurologyindia.com/article.asp?issn=0028-
3886;year=2011;volume=59;issue=4;spage=601;epage=604;aulast=Krishnan
» Abstract
» Introduction
» Case Report
A 21-year-old male presented with intractable seizures since the age of 8 months. He had
infantile spasms at the onset and used to have disabling multiple seizure types: Left focal
seizures with secondary generalization, sudden head and trunk flexion associated with
falls and injuries, and atonic seizures since the age of 2 years. The preoperative seizure
frequency was two to three times per week, mostly in clusters at any time of the day. He
had delayed motor milestones and attained walking at 2 years and language at 3 years.
Left hemiparesis was noted at 2 years of age. However, the patient was independent for
activities of daily living.
On neurological examination, he had left hemiparesis (4/5) with mild hand grip weakness
and was ambulant. Neuropsychological evaluation showed below average IQ of 48 and a
Social Quotient of 52 with behavioral problems. Ictal EEG showed epileptiform
discharges with right hemisphere hemispherical onset. Magnetic resonance imaging
(MRI) of brain showed an extensive right hemispheric polymicrogyria [Figure 1] and
[Figure 2]. Blood oxygen level dependent (BOLD) functional MRI (fMRI) with self-
paced sequential finger tapping and ankle dorsiflexion paradigms revealed lateralization
of bilateral upper and lower limb motor functions to the normal left hemisphere [Figure
3] and [Figure 4]. The patient underwent a right frontoparietal craniotomy and vertical
parasagittal functional hemispherectomy as described by Delalande. Postoperatively, the
patient did not have any worsening of his pre-existing deficits and has been seizure free
(Engels Class I outcome) for more than 1 year.
» Discussion
For a functional motor shift to the normal hemisphere to happen, the innate capacity of
neural plasticity would be the key. Neural plasticity is a change in functional destination
of the existing neurons, that is, a reorganization of the remaining cortical-subcortical
networks and their descending projections and does not involve the generation of new
neurons. The basis of neural plasticity derives from synaptic plasticity. Synaptic plasticity
refers to changes in the strength of neurotransmission induced by activity experienced by
the synapse in the past. Changes in the frequency or strength of activation across
synapses can result in long-term increases or decreases in their strength, referred to as
either long-term potentiation (LTP) or long-term depression (LTD), respectively. Neural
plasticity entails increase in new synapses besides strengthening and expansion of
influence by dendritic arborization. For a given neuronal function, there are far more
pathways than actually in use, which become available for the organism by opening up of
dormant synapses by decrease in inhibition, increased excitability or decreased threshold
of synaptic transmission. Damage to a functional area of the brain also causes loss of
suppression to an associated/dormant remote area of the brain as per the theory of
Diaschesis. After hemispherectomy the inhibition of the corpus callosum is stopped,
hence the ipsilateral pathways can open up. Also existent is an overall hyperexcitability
(also increase in neuromodulators and neurotrophins) noted after such cortical insult. This
overall hyperexcitability helps neuroplasticity.
This capacity of plasticity has a limiting window of opportunity which is to do with the
end point of plasticity. Plasticity is postulated to occur till 7 years for language, between
5 and 16 years for frontal lobe functions and between 1and 11 years for occipital
functions. The corpus callosum suppressive nature on the ipsilateralcorticalspinal
projections is maximally completed by 10 years of age. This means delay would close the
capacity of plasticity which is needed to reverse postoperative weakness. Early surgery
results in better cognitive outcome by reducing the seizure-induced damage of normal
hemispheric development. Also, in certain hemispheric epilepsy syndromes like
Rasmussen's encephalitis and extensive Sturge Weber syndrome, progressive extensive
hemispheric deficits occur; hence, early hemispherotomy is indicated before maximal
deficit with gains in neurocognitive outcomes. Having said this, gains in neurocognitive
status are possible following hemispherotomy for late onset seizures andin patients with
worsening focal motor deficits as a wide age range has been noted for interhemispheric
transfer of language and motor function. Post hemispherectomy re-organization begins
soon after surgery but can continue for as long as 1 year. Our patient presented with mild
left-sided weakness with intact gross motor and fine motor activity much later than the
stipulated time for plasticity capacity. Such patients are known to be more susceptible to
have significant postoperative weakness. An fMRI, however, showed a complete shift of
the motor function to normal hemisphere. This precluded his chances of postoperative
deterioration.
The exact prevalence of shift of motor and language functions in response to congenital
and acquired insults is not known. Several techniques such as intracarotidamobarbital test
(Wada test), positron emission tomography, fMRI, diffusion tensor imaging (DTI),
transcranial magnetic stimulation (TMS) and near infrared spectroscopy have been used
to assess such shifts in individual patients. Among these, fMRI is the most popular,
considering its wider availability and non-invasive nature. Till the results of careful
longitudinal studies in patients with well-defined lesions and specific deficits are
available, results of fMRI should be interpreted in light of other studies. Specifically, a
combination of fMRI information with DTI fiber tracking or TMS may prove more
accurate for this purpose.
Intractable seizures since the age of 8 months. He had infantile spasms at the
onset and used to have disabling multiple seizure types: Left focal seizures with
secondary generalization, sudden head and trunk flexion associated with falls and
injuries, and atonic seizures since the age of 2 years. The preoperative seizure
frequency was two to three times per week, mostly in clusters at any time of the day.
He had delayed motor milestones and attained walking at 2 years and language at 3
years. Left hemiparesis was noted at 2 years of age.
3. How was the family affected by what happen or who was affected?
It was the 21 year old male, other than that there was none specified.
4. What kind of treatment was given?