Initial Onset of Symptoms Initial Visit August 13, 2010 Patient is a 35 year-old woman Blood pressure, heart rate and weight all fall within a healthy range. She is complaining of fatigue, insomnia, and feelings of depression for approximately 4 weeks. Gave patient The Hamilton Depression Rating Scale
(HAM-D) Her score was 17 which indicates Moderate Depression Ran Basic Metabolic Panel (BMP) and Complete Blood Count (CBC). All results were normal. Diagnosis Patient is diagnosed with Clinical Depression A major depressive episode occurs with symptoms that last for most of the day, nearly every day for at least two weeks. A symptom must either be 1) depressed mood or 2) a noticeable decrease in interest or pleasure in all or most activities. At least
four (or more) additional symptoms are present: significant weight loss / weight gain or decrease / increase in appetite difficulty sleeping or increase in sleeping excessive movement or slowing down associated with mental tension (observed by others) fatigue or loss of energy feeling worthless or excessive guilt difficulty thinking, concentrating or making decisions repeatedly thinking about death or suicide, trying to attempt suicide or having a specific plan to commit suicide Treatment
Patient is prescribed Celexa (Citalopram) 20mg daily. Citalopram is used to treat depression. Citalopram is in a class of antidepressants called selective serotonin reuptake inhibitors (SSRIs). It works by increasing the amount of serotonin, a natural substance in the brain that helps maintain mental balance. Patient is advised that it may take up to 4 weeks to feel full benefits of Citalopram. Patient is advised to call immediately if side-effects are present Scheduled follow up appointment in 4 weeks
Follow Up Visit-September 23 Gave patient the The Hamilton Depression Rating Scale (HAM-D) Her score was 20 which indicates Severe Depression She states her depression is getting worse and she is starting to feel confused and forgetful. Dosage of Citalopram is increased to 40mg daily Referred to psychiatrist for further analysis and treatment. Will forward medical records to Dr. Powell.
Psychiatrist 6 weeks after initial PCP visit Psychiatric Referral Patient was referred by primary care physician No improvement after depression medication On medication for 4 weeks Noticeable change in behaviors
Psychiatric Review Meet with patient for 3- 1 hour session Observed Sudden mood changes Extreme paranoia Occasional delusions Occasional short term memory loss
Reviewed mental health family history 1 case of schizophrenia (grandmother) Psychiatric Diagnosis/Treatment Schizophrenia Treatment Prescribed Clozaril Provided patient with a mental health journal Continue therapy once a week
Continued Therapy and Treatment Week 2 Attended all sessions Very frustrated Felt no improvement since starting new medication Paranoia Some jerky movements Journal completed Disturbing thoughts Possible delusions
Recorded taking medication Week 3 Extreme paranoia Insomnia
Increased delusions increased jerky movements Noticeable loss of memory Husband had to remind about last 2 sessions Did not remember my name Reported feeling forgetful Poor general appearance Treatment Continued Determined overall mental health had declined
Immediately referred to hospital for a CT scan noninvasive Combines special x-ray equipment with sophisticated computers multiple images of the inside of the body. cross-sectional images of the area are studied CT Scan Results CT Scan Results Observed a normal CT scan
No white masses Midline appeared normal Unsure of next treatment option Referred to neurologist Neurologist 4 months after initial PCP visit Neurologist Review Referred by Psychiatrist
Date of Appt: 12/3/2010 Signs of dementia Memory loss Very frustrated with medicines Paranoia Tremors/uncontrollable jerking Conditions to Check Alzheimers
Huntingtons Disease Parkinsons Week 1: Dec. 3, 2010 MRI was ordered. Patient is exhibiting parkinsonism. EEG was also ordered to rule out any type of tumor or swelling in the brain. Physical examination was done to measure movement, coordination, and balance.
Patient has difficulties with balance. Speech is slurred. Reflexes were tested and they are very slow. Patient also exhibits tremors. Parkinson symptoms - tremors - slowness of movement - limb stiffness - difficulties with balance - difficulties walking
Test Results Week 1 MRI the MRI showed atrophy of the brain. This is not typical of Parkinson patients. There were also spongy areas within the brain forming. There were not any tumors sighted EEG this test did not show any signs of tumors or swelling in the brain.
Patient MRI Possible Huntingtons Disease WEEK 2: Dec 10, 2010 Patient is adopted, so there is not any prior family history known. Huntingtons is a dominant genetic disorder occurs between ages 30-50. Blood test was done for Huntingtons disease. Blood test is most valid with individuals who have above 40 repeated
gene sequences of CAG on chromosome four. If an individual has less than 30 repeats, there is a less than 1% chance that they will inherit the disorder. Patients test came back negative. Without knowing gene sequence; it is probable that she does not carry Huntingtons. There is a less than 1% chance that she has this disorder. .
Symptoms of Huntingdons: Involuntary jerking Slow, fine movements Difficulty swallowing Impaired gait, posture, and balance Difficulty concentrating Depression MRI shows atrophy of the brain. Week 5: January 5, 2011
Diagnosis is dementia due to Alzheimers. - Tactual Performance Test left hand was mild impaired. - Right-hand performance was much worse. (severe impairment range) -Recall test: 14 out of 50 details. After 30 minutes, no recall of any of the material. MRI does show atrophy and increased white matter
which is consistent with Alzheimers. Prescribed Namenda to help with symptoms. Had her stop taking Clozaril. Week 7: January 19, 2011 Patient has deteriorated rapidly. - Word-finding problems
became increasingly severe. - Finger movements substantially slower - Depression and sleep disturbances intensified Follow up EEG ordered. Prescribed Elavil and Temazepam for depression and insomina.
Week 9: February 2, 2011 Rapid deterioration Restlessness Lack of communication and then became mute Visual hallucinations Week 11: February 16 One- step commands could be followed early in week.
EEG - showed abnormalities with brain signals Week 13: March 2, 2011 Patient became comatose. Week 15: March 17, 2011 Patient is deceased Because of rapid
progression of systems an autopsy has been ordered. Any prion diseases should be investigated. Medical Examiner 7 months after initial PCP visit Autopsy Report
A recommendation to perform an autopsy was received by Johns Hopkins March 18, 2011.The patient presented with symptomology indicating a possible prion disease perhaps Creutzfeldt-Jakob Disease or commonly known as Mad Cow Disease. The autopsy was performed on March 19, 2011 at John Hopkins Medical Laboratories. The lab was prepared with the special precautions because of the nature of the suspected illness. Autopsies cannot be performed at many institutions because of the transmissible nature of the disease. Increased educational efforts, specific protocols, and additional testing sites are needed to address these obstacles, because enormous efforts are currently required to arrange for an autopsy to confirm the diagnosis. Autopsy of a patient with suspected Creutzfeldt-Jakob disease (CJD) requires
unique, special procedures. In cases in which CJD may be present, the autopsy should be limited to the brain and lymphoid tissues. In exceptional cases in which the importance of clinical questions about other organs necessitates that those organs be examined before it is safe to do so, additional tissues may be harvested. A full and complete autopsy was performed. Results of Autopsy The autopsy involved thorough examination of the brain. Which presented as neuropathologic features including neuronal loss, proliferation of glial cells, absence of an inflammatory response, and the
presence of small vacuoles within the neutrophils, which produces a spongiform appearance. The most severe changes were observed in the cerebral cortex. Neuron loss was also substantial in the anterior lateral region of the occipital cortex. The cerebellum was not effected. Comparison of Images of the Brain Mad Cow vs. Normal Mad Cow
Histology Mad Cow Tissue Healthy Tissue What Research Is Taking Place? Many researchers are studying CJD. They are examining whether the transmissible agent is, in fact, a prion or a product of the infection, and are trying to discover factors that influence prion infectivity and how the disorder damages the brain. Using rodent models of the disease
and brain tissue from autopsies, they are also trying to identify factors that influence susceptibility to the disease and that govern when in life the disease appears. They hope to use this knowledge to develop improved tests for CJD and to learn what changes ultimately kill the neurons so that effective treatments can be developed. Disease Overview Mad Cow Mad Cow Disease aka. Variant Creutzfeldt-Jakob Disease
Cause: Prions in the brain are misfolded proteins which replicate by converting their properly folded counterparts. This is what is responsible for the spongy appearance of the brain tissue. This is an infectious disease. In the case of Elizabeth Jersey, she ate infected meat at some point. Systems affected: Nervous: depression, rapid deterioration of mental state, dementia, hallucinations, memory loss, change in personality Digestive: begins to affect swallowing Muscular: deterioration of brain tissue affects signals sent to muscles resulting in tremors, difficulty walking, jerky
movements All systems begin to shut down, resulting in death.
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