One - Discussion Part
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This week's graded topics relate to the following Course Outcomes (COs). 1 Analyze pathophysiologic mechanisms
... [Show More] associated with selected disease
states. (PO 1) 2 Differentiate the epidemiology, etiology, developmental considerations,
pathogenesis, and clinical and laboratory manifestations of specific
disease processes. (PO 1) 3 Examine the way in which homeostatic, adaptive, and compensatory
physiological mechanisms can be supported and/or altered through
specific therapeutic interventions. (PO 1, 7) 4 Distinguish risk factors associated with selected disease states. (PO 1) 5 Describe outcomes of disruptive or alterations in specific physiologic
processes. (PO 1) 6 Distinguish risk factors associated with selected disease states. (PO 1) 7 Explore age-specific and developmental alterations in physiologic and
disease states. (PO 1, 4)
Discussion
Discussion Part One (graded)
• What is your differential diagnosis?
• What tests do you order?
• An MRI comes back and there seems to be a lesion in the temporal lobe does this change
your differential? The EEG also comes back with unusual excitatory activity. What is your
definitive diagnosis? In retrospect did anything bias your first differential?
Responses
6/Rechel DelAntar 12/2016 12:44:25 PM
Differential Diagnosis
Hello professor and Class,
Differential Diagnosis
This is a case of a patient who was previously seen in the mall looking homeless in physical
appearance who exhibits repetitive movement such as “walking to a table, sitting up, walking to a tree
and urinating” oblivious to the people around him and his surroundings. Upon initial exam he has no
recollections of previous events. Based on this history, we may consider:
Seizures = specifically Complex Focal seizure (temporal or psychomotor seizure)with a simple partial
onset followed by impairment of consciousness. In this type of seizure, the patient is able to interact
with the environment with a purposeful, although inappropriate movement. Most characteristic event of
this type of seizure is the automatism; common examples of automatisms are lip smacking, chewing,
facial grimacing, swallowing movements, and patting, picking, or rubbing oneself or one’s clothing. The
body may stiffen but the patient will continue to perform complex activities of which they are involved in
such as driving. Witnesses may not recognize that anything is wrong. Temporal lobe seizures generally
last 11 seconds to 8 minutes (average 2 minutes) and are followed by several minutes of postictal
confusion (McCance, K.L., 2013).
Diagnostic testing = Laboratory studies have to be done to rule out potential causes or triggers to
seizures. MRI of the brain can be performed to check if structural lesions are causing the seizure event
and is helpful in assessing temporal seizures. Temporal lobe seizures commonly result from damage to
specific areas in that part of the brain. This can be due to a head injury, infection, or damage to a portion
of the temporal lobe due to lack of oxygen, brain tumors, genetic syndromes, or lesions of any sort.
Many of these problems also produce brain-tissue scarring called mesial temporal sclerosis. EEG within
24 hours is more sensitive for diagnosing epileptiform abnormalities as it is able to localize seizure focus.
Brain cells communicate with each other and produce our consciousness, thoughts, and actions by
electrochemical processes. Certain patterns of electrical activity disrupt this normal function of the brain
and spread in abnormal patterns within the brain. This process can be seen on an EEG (Walter, B.,
2013).
With the patient’s MRI results coming back with temporal lobe lesion and an EEG reading of
unusual excitatory activity, my differential diagnosis remains the same. The results support the
diagnosis. In retrospect, the patient’s inability to recollect his actions made me think that he was not in
control of his actions and also reminded me of post ictal stage of seizure when patients were unable to
recall the seizure event is what gave bias to my differential diagnosis.
References:
McCance, K. L., Huether, S. E., Brashers, V. L., & Rote, N. S. (2013). Pathophysiology: The
biologic basis
for disease in adults and children (7th ed.). St. Louis, MO: Mosby.
Walter, B. (2013). Bradley’s neurology in clinical practice (6 ed.). Philadelphia, PA: Elsevier,
Saunders.
th
Instructor Brown reply to Rechel DelAntar 6/14/2016 2:23:24 PM
RE: Differential Diagnosis
What symptoms are possible with right vs. left side lesion?
6/Rechel DelAntar reply to Instructor Brown 14/2016 10:20:29 PM
RE: Differential Diagnosis
Hello Professor and Class,
Right side vs. Left side lesion
The brain is the control center for all human activity, including vital processes
(breathing and moving) as well as thinking, judgment, and emotional reactions. Brain lesions
can be caused by injury, infection, exposure to certain chemicals, problems with the immune
system, and more. Typically, their cause is unknown. Symptoms experienced by the patient
vary depending on the location, type and size of the lesion. The brain is divided into two halves
(hemispheres). The left half controls movement and sensation in the right side of the body, and
the right half controls movement and sensation in the left side. Therefore, damage to the right
side of the brain may cause movement problems or weakness on the body's left side. For
majority of the population, the left half of the brain is responsible for verbal and logical functions
including language (listening, reading, speaking, and writing), thought and memory involving
words. Patients with this type of lesion will exhibit right side weakness, aphasia, slow speech and
decreased attention span. The right half is responsible for nonverbal and intuitive functions such
as putting bits of information together to make up an entire picture, recognizing oral and visual
patterns and designs (music and art), and expressing and understanding emotions. Patients
with this type of lesion will exhibit left sided weakness, will have difficulty with complex
communication such as difficulty identifying relevant information, inability to interpret body
language and relevant information. They tend to be very literal in their interpretation of things
and situations. Left hemispheric damage may produce a right hemianopsia or quadranopsia.
They have flat affect and at times are impulsive (Novack, T., n.d.). Right Hemispheric damage
may not only produce a left homonymous hemianopsia or quadranopsia, but it may also produce
a severe attention disorder to the left side called left hemispatial inattention or visual neglect.
Spatial orientation, body position and nonverbal communications may become impaired in some
individuals. Emotional and behavioral problems may occur. Thinking skills may be effected.
Meanwhile, many patients will be unaware of the full extent of their impairment. They may even
deny they have a problem (Manasco, H., 2014).
References:
Manasco, H. (2014). Introduction to neurogenic Communication Disorders.
Burlington, MA: Jones and Bartlett Learning.
Novack, T. (n.d.). Understanding TRI part 2: Brain Injury Impact on Individual
Functioning. Retrieved from http://www.msktc.org/tbi/factsheets/
Understanding-TBI/Brain-Injury-Impact-On-
Individuals-Functioning.
Brittany Heller 6/12/2016 1:51:25 PM
AD
"Alzheimer disease is a neurodegenerative disorder of uncertain cause and pathogenesis that
primarily affects older adults and is the most common cause of dementia" ( Wolk & Dickerson, 2016, p.
1). AD typically affects patients older than 60 years and is rarely occurs in less than 60 (Wolk &
Dickerson, 2016, p. 1). Some have suggested that there is a mutation in genes that alter beta-amyloid
protein production and metabolism (Wolk & Dickerson, 2016, p. 1). Genes that are mutated include
APP, PSEN1, and PSEN2 (Wolk & Dickerson, 2016, p. 1). AD also had three common areas of cortical
thinning patterns that were observed which are the medial temporal, diffuse, and patietal dominant
atrophy subtypes (Hwang, Kim, Jeon, Lee, HOne, Roh, Lee, Koh, & Noh, 2016, p. 1). The thinning of the
cortical areas may suggest a predictive pattern in the pathophysiology of AD. Memory impairment is the
most common symptom of AD. "Executive dysfunction and visuospatial impairment are often present
relatively early, while deficits in language and behavioral symptoms often manifest late in the disease
course" (Wolk & Dickerson, 2016, p. 2). Other symptoms can include executive function and
judgement/problem solving, behavioral and psychological symptoms, apraxia, olfactory dysfunction,
sleep disturbances, and seizures ( Wolk & Dickerson, 2016, p. 5).
After completing a standardized mental status scale, the first test I would order would be an MRI. "Brain
MRI can document potential alternative or additional diagnoses of cerebrovascular disease, other
structural disease, and regional brain atrophy suggesting frontotemporal dementia or other types of
neurodegenerative disease" ( Wolk & Dickerson, 2016, p. 6).
If the MRI came back with a lesion in the temporal lobe, this would not change my diagnosis. "The
most characteristic focal finding in AD is reduced hippocampal volume and medial temporal lobe atrophy"
(Wolk & Dickerson, 2016, p. 6). Seizures are one of the clinical manifestations that can be present in
AD. "Temporal lobe epilepsy is the most common form of partial or localization related to epilepsy"
(Holmes, Sirven, & Fisher, 2013, p. 1). For temporal lobe seizures, an EEG would be essential for
diagnosing purposes. On an EEG, sharp waves or spikes would be seen showing unusual activity
(Holmes et al., 2013, p. 4).
After thinking about this diagnosis, the memory loss was a key factor in deciding on the AD diagnosis.
Due to his repetitive actions, I thought he could possibly have OCD as well. Not having the age of the
patient also made this difficult to diagnosis this. Not recognizing the police also had a judgement
impairment which leaned more towards AD as well.
Holmes, G., Sirven, J., & Fisher, R. (2013). What is temporal lobe epilepsy? Epilepsy Foundation.
Retrieved at: http://www.epilepsy.com/learn/types-epilepsy-syndromes/temporal-lobe-epilepsy
Hwang, J., Kim, C., Jeon, S., Lee, J., Hong, Y., Roh, J., Lee, J., Koh, J., 7 Na, D. (2016) Prediction of
Alzheimer's disease pathophysiology based on cortical thickness patterns. Alzheimers Dementia, 2, 58-
67. doi: 10.1016/j.dadm.2015.11.008. Retrieved at: http://www.ncbi.nlm.nih.gov/pubmed/27239533
Wolk, D., & Dickerson, B. (2016). Clinical features and diagnosis of Alzheimer Disease. UpToDate.com.
Retrieved at: http://www.uptodate.com/contents/clinical-features-and-diagnosis-of-Alzheimer-disease?
topickey
Lanre Abawonse reply to Brittany Heller 6/14/2016 8:46:21 PM
RE: AD
Brittany, your narration is great. I would like to add some few points to your diagnosis
and the findings on the magnetic resonance imaging MRI. Just as you selected Alzheimer’s
disease as your number diagnosis, I did the same on my selection. Alzheimer’s disease is one
of many conditions that are worth putting into consideration when patients have results that
indicate temporal lobe lesions. The consideration of symptoms can also include alcoholism and
substance abuse etc. Upon further study of temporal lobe lesions resulting effects on patients,
it has been suggested that there are a behavioral changes in these patients. Gudmundsson et.
al., (2015) suggested that cortical atrophy, indicating neurodegeneration, is commonly seen on
imaging of the aging brain of a patient who has temporal lobe lesions on MRI. In addition,
cortical atrophy may also be an expression of small vessel disease. Prospective populationbased
studies using magnetic resonance imaging (MRI) report that white matter changes
increase the risk of subsequent dementia. With these findings, it could suggest that this patient
is going through behavioral changes and this is evidenced by the patient’s lack of insight along
with memory impairment.
Gudmundsson, P., Olesen, P. J., Simoni, M., Pantoni, L., Östling, S., Kern, S., & ... Skoog, I.
(2015). White matter lesions and temporal lobe atrophy related to incidence of both
dementia and major depression in 70-year-olds followed over 10 years. European
Journal Of Neurology, 22(5), 781-e50.
6/Jonathan Bidey reply to Brittany Heller 17/2016 12:20:14 PM
RE: AD
Brittany,
Excellent post! You did a wonderful job describing which genes are involved with
Alzheimer’s disease (AD). You also did a wonderful job describing the physical changes
which occur in the brain during AD. I particularly enjoyed your description of the use of
MRI in diagnosing AD. You mentioned hippocampal volume and its correlation to AD.
MRIs are not only used to evaluate hippocampal findings, but also to assess for other
potential causes of symptoms (Li et al., 2014). Studies are suggesting that changes in
hippocampal volume may soon be able to be detected before any symptoms or memory
loss has occurred. By assessing for these changes early on, prior to the onset of disease,
it is possible that therapies will be designed to slow the onset for those at risk (Li et al.,
2014). Excellent post!
-Jonathan
Reference:
Li, M., Oishi, K., He, X., Qin, Y., Gao, F., & Mori, S. (2014). An efficient
approach for differentiating Alzheimer's disease from normal elderly based
on multicenter MRI using gray-level invariant features. PLoS ONE, 9(8),
1-13. http://dx.doi.org/10.1371/journal.pone.0105563
Lorna Durfee 6/13/2016 6:35:51 AM
Discussion Part One
Scenario:
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Repetitive urination, agnosia, aphasia, apraxia, lesion in temporal lobe?
What is your differential diagnosis?
• What tests do you order?
• An MRI comes back, and there seems to be a lesion in the temporal lobe does this change
your differential? The EEG also comes back with unusual excitatory activity. What is your
definitive diagnosis? In retrospect did anything bias your first differential?
Doctor Brown:
DIFFERENTIALS:
Differential #1: Head trauma, with brain injury, traumatic brain injury with cognitive dysfunction
Differential #2: Brain dysfunction.
Differential #3: Excessive alcohol consumption and Wernicke-Korsakoff Syndrome
Differential #4: Schizophrenia with agnosia.
Differential #5: Temporal lobe epilepsy.
My chosen differential diagnosis is Differential #1: Head Trauma or traumatic brain injury.
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Differential #1: Traumatic Brain Injury or head trauma.
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