Dlb and Patient KM

¶ … medication for patient named KM is Prothiaden. Prothiaden is used to treat depression as well as limit the feelings of anxiety in those taking it. The case file indicates a normal MRI and no previous diagnosis of neurological disorders like Parkinson's disease. Patient KM has complained of depression and anxiety related to the passing of her mother. Progressive functional and cognitive decline has presented ever since mother died four years ago.

Although the patient worked until the age of 60 as an accountant, within the last 18 months patient has experienced fluctuations in mood, confusion, mild word finding difficulties and spatial disorientation. She also has visual hallucinations and violent dreams. She experienced recent falls and a slowing of motor skills. These symptoms extend to the inability to carry out motor sequences with either hand or double alternating hand movements. Although she can detect shapes well, she has poor ability in number location and dot counting.

When instructed to draw a cube, she drew one well. When instructed to draw a cross, she could not form one properly. She could also not draw the time on a clock though she could draw a clock well. Assessment Parkinson's progression takes between 10-20 years. Lewy bodies faster with an 18-month progression as experienced by KM. KM's REM-circadian sleep disorder also points to Lewy The clinical information shows numerous evidence of functional decline, a crucial identifier for dementia. AD can be ruled out from KM's neuropsychological scores.

KM's scores are as follows: the predicted (pre-morbid) IQ rated average for the National Adult Reading Test despite KM's 17 years of education. The Wechsler's Adult Intelligence Scale - III has a maximum score of 10. KM's score of 6 (1.3 sd from the normative data) classifies as borderline and 10 intact. 5 means impaired. The subtests scores for the WAISIII or 'picture completion' is above average, 'similarities' above average, 'comprehension' borderline average, 'block design' impaired, 'digit span' impaired, 'information' intact, 'arithmetic' borderline average.

Her average, above average and intact scores in Wechsler Memory Scale - III rules out AD. There is marked impairment as shown in the Rey Complex Figures. The COWAT score was -6, showing severe impairment. The Colour Form Sort identifies a person's flexible thinking ability to which KM did not do thus showing significant impairment. The Trail Making Test for part A was impaired, and for part B was discontinued. The Depression, Anxiety and Stress Levels indicate possible toxicity to the hippocampus, which can cause dementia.

The physical assessment involving drawing a time on the clock and the patient's inability to interpret visual information showed mixed results. She sees the clock and may see the numbers but cannot put the hands on the clock to tell the time. The lowest raw scores in mental control (11) and visual reproduction % retention (8) as well as digit span (7) and block design (4). Patient also indicated having vivid hallucinations like "elephants in the house." She acts out her violent dreams and forgets things demonstrating confusion. Her falls indicate potential neurological problems.

Differential Diagnosis Several main neurodegenerative conditions share parkinsonian features. These features may be bradykinesia, tremor, rigidty, and gait disturbances (Gaddipati and Umaiorubahan, 2014). Such disorders have multifaceted clinical presentations reflecting degeneration in numerous neuronal systems. Nevertheless, because of the mutual parkinsonian features, the illnesses have been jointly named Parkinson-plus syndromes. People with these conditions frequently have a history of responding poorly to standard treatment protocols for Parkinson disease.

An insufficient response to treatment within a patient presenting parkinsonian symptoms suggests possibility of a Parkinson-plus condition warranting a search for the symptoms and signs of degeneration within other neuronal systems (Hohler and de Leon, 2011, p. 1860). In adding to lack of reaction to dopamine or carbidopa/levodopa (Sinemet) agonists in the early phases of the illness, other clinical signs indicative of Parkinson-plus conditions include the following: 1. Early onset of postural unsteadiness 2. Early onset of dementia 3.

Early onset of psychosis or hallucinations with low dosages of dopamine or carbidopa/levodopa dopamine agonists 4. Visual signs, such as diminished vertical gaze, nystagmus, blinking on saccade, blepharospasm, as well as apraxia of eyelid closure or opening, square-wave jerks 5. Pyramidal tract signs unexplainable by earlier spinal cord lesions or stroke 6. Autonomic symptoms like postural incontinence and hypotension early in the course of the illness 7. Prominent motor apraxia (Mark, 2001, p. 609). Modern immunocytochemical methods and genetic results propose that Parkinson-plus syndromes can be classified into two types: tauopathies and synucleinopathies.

Clinically though, researchers have identified five separate Parkinson-plus conditions as follows: 1. Progressive supranuclear palsy 2. Multiple system atrophy 3. Corticobasal ganglionic degeneration 4. Parkinsonism-dementia-amyotrophic lateral sclerosis complex 5. Diffuse Lewy body disease (Verstraeten, Theuns and Van Broeckhoven, 2015, p. 143). CBGD or Cortical basal ganglionic degeneration is a sporadic neurodegenerative tauopathy. It can be seen as both a condition of distinguishing movement as well as cognitive dysfunction such as corticobasal syndrome, plus a medically defined illness.

One defines the corticobasal syndrome by progressive dementia, limb apraxia, and Parkinsonism; however, these may happen because of a sum of pathologic bodies (Armstrong et al., 2013). The most typical are Pick complex disorders, but Alzheimer disease plus even rare disorders (Niemann-Pick type C and CNS Whipple disease) can be related with corticobasal disease. Histopathologically recognizable CBGD can also show clinically as primary progressive apraxia or primary progressive aphasia or in patients that presented no prominent movement disorders formerly in their lives.

Additional Investigation DAT imaging may provide a more accurate diagnosis for DLB. This is because those with DLB tend to have lower levels of DAT or dopamine transporter protein as shown in a 2015 article written by McCleery et al. People with DLB have reduced levels of the dopamine transporter protein (DAT) in a part of the brain known as the corpus striatum. It is possible, using tracers that bind to the dopamine transporter, to identify this reduction on certain brain scans (PET or SPECT scans).

This is known as DAT imaging (McCleery et al., 2015, p. 1). Along with DAT imaging, other techniques for diagnosis could yield more information and help eliminate other conditions like Alzheimer's disease through identification of tangle pathology. Lewy body staging in the latest research articles is linked with the occurrence of persistent visual hallucinations as well as persistent delusions.

All standard psychiatric features were considerably more recurrent in DLB than in Alzheimer's disease, "as were persistent visual hallucinations, but patients who had dementia with Lewy bodies and severe tangle pathology had a clinical symptom profile more similar to that of Alzheimer's disease patients and were less likely to have neocortical Lewy bodies" (Ballard et al., 2004, p. 843). Other things to look for aside hallucinations in early symptoms of DLB is depression and anxiety as these appear as major indicators along with halluncinations.

"Impairments of working memory and visuospatial functions, visual hallucinations, and depression (or symptoms of depression such as apathy and anxiety) have been identified as early indicators of DLB" (Simard, van Reekum and Cohen, 2000, p. 425). Other things to consider to augment diagnostic accuracy in cases of suspected DLB is inclusion of REM sleep behavior disorder as research shows its connection to some of the symptoms experienced early on in patients with DLB. "Inclusion of RBD as a core clinical feature improves the diagnostic accuracy of autopsy-confirmed DLB" (Ferman et al., 2011, p. 875).

Intervention Plan Dementia with Lewy bodies or DLB is a neurodegenerative condition with characteristics of progressive cognitive decline and at least two of the resulting symptoms: visual hallucinations and cognitive fluctuations, or Parkinsonism. Although DLB affects over one million people in the United States alone each year, there exists no U.S. Food and Drug Administration -- approved treatments for patients suffering from DLB. Furthermore, there is limited to no basis of research for direct treatment.

Unreliable evidence and partial studies point to the use of memantine and cholinesterase inhibitors as possible effective treatment possibilities for individuals with DLB (Burke et al., 2012) & (Rolinski et al., 2012). Some nonpharmacological approaches like physical, voice, and occupational therapy, can be valuable treatment options for patients with DLB. One such occupational therapy technique that has seen success in treating patients with DLB is STOMP or Skill-building through Task-Oriented Motor Practice.

"Our findings suggest that STOMP has the potential to serve as a structure for the evaluation and treatment of occupational performance deficits in people with dementia" (Ciro, Hershey and Garrison, 2013, p. 556). Training practices like this enable those with DLB to practice cognitive skills and keep muscle memory. Other practices such as mirror image recognition and voice therapy enable patients to regain certain abilities loss due to illness and enables a decrease in confusion and memory loss (Gil-Ruiz et al., 2013, p. 1).

Medications exist to help with DLB sufferers with hallucinations and confusion. Acetylcholinesterase inhibitors, like galantamine (Reminyl), donepezil (Aricept), or rivastigmine (Exelon), can help diminish hallucinations, drowsiness, and confusion in some people. Clozapine, used to treat schizophrenia, can also help diminish hallucinations. These medications work through increasing levels of the acetylcholine within the brain, thus improving the ability of brain cells to send signals more effectively to each other. The best medication for KM would be Clozapine.

References Armstrong, M., Litvan, I., Lang, A., Bak, T., Bhatia, K., Borroni, B., Boxer, A., Dickson, D., Grossman, M., Hallett, M., Josephs, K., Kertesz, A., Lee, S., Miller, B., Reich, S., Riley, D., Tolosa, E., Troster, A., Vidailhet, M. and Weiner, W. (2013). Criteria for the diagnosis of corticobasal degeneration. Neurology, 80(5), pp.496-503. Ballard, C., Jacoby, R., Del Ser, T., Khan, M., Munoz, D., Holmes, C., Nagy, Z. and Perry, E. (2004). Neuropathological Substrates of Psychiatric Symptoms in Prospectively Studied Patients With Autopsy-Confirmed Dementia.