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Cognitive Impairment

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Cognitive Engineering, LLC

Cognitive Engineering can provide testing channels to help you, your family member or your client determine whether they have signs of Alzheimer's disease, dementia, or cogntive impairment, and to what degree.

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, Lyme disease

     Illicit drugs

     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.

n      Written Neuropsychiatric Evaluation Tools – These are standard, and of relatively good quality, but certainly can be open to manipulation by the examinee.

     Mini Mental Status Exam

     Mattis Dementia Rating scale

     Mindstreams™ (NeuroTrax Corp., NY)

     ADAS-cog

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:

     Hyperintense 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.

n      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.

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

*      MRI,

*      Generation of an expert report on the etiology of symptoms, which incorporates the principles of causation and scientific evidence.