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Mild
cognitive impairment (MCI), a perceivable decrease in thought
processes, primarily memory, occurs in individuals who are otherwise
able to function in everyday activities.
These patients have difficulty remembering the names of people,
performing calculations, navigating in a mall parking lot, and
keeping track of common objects. Various levels of self-awareness of
these handicaps may exist, and complex systems of compensation can
be constructed. MCI can affect a persons ability to work, to
function independently, and perform activities of daily living
(ADL), particularly if the loss progresses. Written testing and
neurologic evaluation are important methods of evaluation, and
neuroimaging has taken on a greater role in documenting the presence
of MCI.
Most (but not all)
patients with MCI develop a progressive decline in their thinking
abilities over time, and neurologic diseases are often the
underlying cause. Occasionally, a patient may experience MCI as a
result of toxin exposure in the workplace, trauma, prescription
medication or ither reversible neurologic conditions such as NPH.
This can lead to a claim for damages, and the presence, degree, and
prognosis of the MCI can then become an important component of the
litigation development.
The diagnosis of
MCI relies on the fact that the individual is able to perform all
their usual activities successfully, without more assistance from
others than they previously needed. In this regard, MCI is different
from dementia, where memory loss and at least one other cognitive
deficit has progressed to such a point that normal independent
function is impossible and the individual can no longer successfully
manage their finances or provide for their own basic needs.
Of interest, MCI may in some persons be a precursor to AD.
Therefore, screening for MCI may be an important component of workup
for early AD. MR Spectroscopy is one methodology which provides an
objective means of screening for and quantifying neurodegenerative
processes that can cause age-dependent cognitive deficits which can
eventually lead to AD and other dementias.
Common causes of MCI
include:
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Multiple infarct dementia
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Cerebral Ischemia – stroke,
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Post-Trauma – concussion,
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Medication - interferon, SSRI,
hypnotics; Ambien, NSAID, opioid analgesics, neuroleptic
antipsychotics,
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Neurodegenerative illnesses -
Alzheimer disease (AD) and other dementias,
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Hypoxic – decompression,
post-resuscitation,
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Metabolic: hypothyroid, B12
deficiency
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Normal pressure hydrocephalus
(NPH),
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Treatable intracranial masses –
subdural hematoma (SDH),
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Imprisonment, torture, sensory
deprivation, chronic pain
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Toxic chemical exposure
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Infections – HIV, Hepatitis C,
neurosyphilis, Lyme disease
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Illicit drug use (metamphetamine,
cocaine, THC),
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Inflammatory or immune diseases:
SLE
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Chronic Illnesses – Chronic
Fatigue Syndrome, major organ failure (heart,
lung).
Exposure of a normal brain to a drug
or toxin can result in MCI, of varying intensity and persistence.
Most physicians are well-aware of the ability of chemical toxins,
drugs, disease states and infections processes (some are listed
above) to effect a patient’s cognitive performance. Documenting this
impairment is crucial!
MCI is typically subtle, but it is
measurable. Patients have memory problems greater than normally
expected for their age, but do not show other symptoms of dementia,
such as impaired judgment or reasoning. The injury is thought to
arise mostly in the medial temporal lobe, including the hippocampus,
but can also be widespread, involving a large portion of the
neocortex and subcortical white matter. The indicated evaluation of
MCI will include a comprehension neurologic examination,
neuropsychologic evaluation including formal neurologicpsychologic
testing, electrophysiologic tests when indicated, serologic and CFS
tests (as indicated), and specialty neuroimaging tests. The less
subjective, and the more quantifiable the better.
Evaluation of Cognitive
Impairment
There are a number of reasons why one
needs to measure the degree of cognitive impairment. These include
quantifying the current state, documenting the degree of ongoing
loss, demonstrating the degree of physical or mental impairment,
developing a treatment plan and giving a prognosis. The principle
areas of MCI documentation and workup are discussed above.
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Comprehensive neurologic
exam,
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The neuropsychiatric
interview should always be performed by an experienced
professional, and for medical legal cases, they need to have a
willingness to be deposed and the appropriate skill set for
deposition.
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Written Neuropsychiatric
Evaluation Tools – These are standard, and of relatively good
quality, but certainly can be open to manipulation by the
examinee.
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MRI – provides structural
information on the brain, and can be used to rule out alternative
etiologies. Changes associated with MCI which have been reported
with MRI include:
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Hyperintense lesions in the
periventricular white matter and centrum semiovale on
T2-weighted images.
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These lesions tend to be patchy in
the early stages and diffuse as the disease progresses
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The differential diagnosis
includes multiple sclerosis (MS) and small-vessel disease.
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MR Spectroscopy – identifies
abnormal areas of neuron function, and can make a correlation to
functional deficits in MCI.
-
MRS can analyze for a number of
specific chemicals, including N-acetylaspartate (NAA), a brain
metabolite localized almost exclusively to neurons and neuronal
processes in the human adult brain
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MRS measures changes in the signal
intensity of NAA, which correlates with brain damage
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Can actually quantify
neuronal-axonal injury and loss. The final product is an actual
picture of the damage, a visual representation.

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Functional MR Imaging – used to provide an objective
measurement of a perceived deficit. A stimulus or task is
presented during the actual MR imaging process, and functional
brain activity is monitored.
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Electrophysiologic testing, including EEG.
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Serologic and CSF testing, as indicated.
Issues in demonstrating MCI include establishing the pre-morbid
state of cognition, determining the presence of mental decline, and
linking the mental decline to its cause. It may be difficult to
establish that a normal baseline existed, as injured individuals did
not plan on an injury occurring, and did not take a convenient
snapshot of brain function at various normal points in their lives.
An estimate of cognitive function can be reconstructed, though, by
an independent objective analysis of a persons job and school
performance, samples of their writing, interviews with family and
coworkers, and other forms of scrutiny of their lives pre-MCI.
Utilizing a unified team to definitely evaluate a patient with
failing mental function would be
ideal. The performing center(s) must be experienced in specialized
MR imaging (including MRS and functional MRI), and be proficient in
neurocognitive testing and neurologic evaluation. The evaluating
center should utilize an experienced team of professionals able to
develop a report directed to satisfying the principles of scientific
evidence. Team leaders (neurologist, neuroradiologist, cognitive
scientist and others) must be experienced in and willing to be
deposed.
Conclusions:
A practical clinical program when implemented can determine with
medical probability whether a patient is experiencing Cognitive
Impairment, to what degree, and from what likely causes. Such an
evaluation must depend on valid scientific principles, backed by
studies published in peer-reviewed journals.
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