Mild cognitive impairment (MCI) refers to a perceivable decrease in
thought processes, primarily memory, 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 effect a persons ability to work, to
function independently, and perform activities of daily living (ADL), particularly
if the loss progresses.
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 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. Most (but not all) patients with MCI
develop a progressive decline in their thinking abilities over time, and dementias
are often the underlying cause. Occasionally, a patient may experience MCI as a result of toxin exposure in the workplace,
trauma, or prescription medication. 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.
Common causes of MCI include:
Cerebral Ischemia - stroke
Post-Trauma - concussion
Medication - interferon, SSRI, hypnotics; Ambien,
NSAID, opioid analgesics, neuroleptic antipsychotics.
Degenerative illnesses - Alzheimer and other dementias
Hypoxic – decompression
Chronic Illnesses: SLE, CFS
Imprisonment, torture, sensory deprivation
Toxic chemical exposure
Infections – HIV, Hepatitis C, neurosyphilis,
Inflammatory or immune diseases: SLE
MCI is typically subtle, but it is measurable. Patients have memory problems
greater than normally expected for their age, but does 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. Measures of MCI include a detailed clinical evaluation
by an experienced neuropsychologist, neuropsychologic testing, and specialty neuroimaging tests. The less subjective, and
the more quantifiable the better.
Measurements of Cognitive Impairment
There are a number of reasons why one needs to measure the degree of cognitive imparment. 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. Three principle areas of documentation in the workup of MCI are a thorough neuropsychiatric
interview, written testing, and Magnetic Resonance Imaging (MRI) and Magnetic Resonance Spectroscopy (MRS).
n 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.
Neuropsychiatric Evaluation Tools – These are standard, and of relatively good quality, but certainly can be open to
manipulation by the examinee.
¨ Mini Mental
¨ Mattis Dementia
¨ Mindstreams™ (NeuroTrax Corp., NY)
n 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:
lesions in the periventricular white matter and centrum semiovale on T2-weighted images.
¨ These lesions
tend to be patchy in the early stages and diffuse as the disease progresses
¨ The differential
diagnosis includes multiple sclerosis (MS) and small-vessel disease.
n MRS –
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
¨ MRS measures
changes in the signal intensity of NAA, which correlates with brain damage
¨ Can actually
quantify neuronal-axonal injury and loss. The final product is an actual picture of the damage, a visual representation.
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.
Issues in demonstrating MCI include establishing a normal state
of cognition prior to injury, demonstrating objectively a cognitive impairment, and linking the MCI to the causative agent.
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.
Exposure of a normal brain to a drug or toxin can result in
MCI, of varying intensity and persistence. 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.
Ultimately, in practice, a clinical differentiation of idiopathic Parkinsons from Manganism is a clinical determination
which must include :
Complete review of the medical records,
Occupational History / exposure to Mn,
A complete physical and neurologic exam, including a hepatologic evaluation,
Evaluation by a testifying neurologist,
Targeted neuro-psychiatric testing
Generation of an expert report on the etiology of symptoms, which incorporates the principles of causation and scientific