Diagnosis

1. 1
Mental Health Consultation
Patient Name: Progressive Supranuclear Palsy Facility: XXXX
Date: x-xx-xx
Abbreviated Format: the following sections will not be included in this report: Comprehensive
Background Information, All Current Medications and Complete Medical History: That
information can be found elsewhere in this chart.
Reasonfor Referral: xx-year-old, white, widowed, female… I was asked to evaluate her
“because of a diagnosis of bipolar disorder”. She was admitted from XXX on xx-xx-xx where
she was treated for frequent falls. Documents which accompanied her from XXXX offered a
diagnosis of Progressive Supranuclear Palsy made by her neurologist at Xxxx Neurology.
Excerpts from her XXX DC summary, neurology consult can be seen below:
“had multiple hospitalizations over the past year both at XXXX as well as at XXXX…history of opioid and
benzodiazepine dependence…in her usualstate of health until the past several days when she reports increasing
weakness. …she stood up at home and fell to the ground secondary to significant leg weakness…had some degree of
slurred speech for which CT scan of the head and MRI of the brain were obtained to assess fora stroke. MRI of the
brain was unremarkable other than microangiopathic changes of moderate degree…. No evidence of acute stroke…
with progressive supranuclear palsy likelyexplaining her multiple falls…She has been extensively worked up as
an outpatient”
PARKINSON'S DISEASE HISTORY OF FALLING
CORONARY ARTERY DISEASE
HEART FAILURE BRADYCARDIA
CHRONIC OBSTRUCTIVE PULMONARY DISEASE
TAKOTSUBO SYNDROME
CHRONIC PAIN SYNDROME
OPIOID DEPENDENCE
MAJOR DEPRESSIVE DISORDER, SINGLE EPISODE
NICOTINE DEPENDENCE
GASTRO-ESOPHAGEAL REFLUX DISEASE
OLD MYOCARDIAL INFARCTION HYPERLIPIDEMIA
PROGRESSIVE SUPRANUCLEAR OPHTHALMOPLEGIA
Current medications include: Paroxetine 40MG qd, Trazadone 25mg qhs, Quetiapine Fumarate
50MG qhs, Hydrocodone-Acetaminophen 5-325 MG q 6hr prn, Valium 2MG (Diazepam) qd.
Mental Status Exam: I found her in bed midmorning. She was cooperative and pleasant. Her
affect was appropriate and her mood was within normal limits. Her speech was coherent and
relevant. When I questioned her about manic symptoms she responded, “I babble for a day and
then it stops”. “I was hospitalized long ago at the XXX, it was xxx there, but more recently I was
hospitalized at XXXX”. She said she was divorced with three adult sons. “My sister is a paranoid
schizophrenic and lives in a group home; I live with my brother in Xxxxxx and will be going back
there”. She said, she hasn’t taken a mood stabilizer since she took Lithium a long time ago “I
didn’t like it”. There were no overt delusions or hallucinations. Her insight and judgment
appeared to be intact. She was alert and fully oriented with a clear sensorium. She said, “I like it
here; this place is like a safety net”.

2. 2
Findings: She did not provide any history which was consistent with Bipolar Disorder nor was
it evident in her MSE but this issue pales in comparison to the question of Progressive
Supranuclear Palsy (PSP) which is a neurodegenerative disease whose characteristics include:
supranuclear ophthalmoplegia, which first restricts downward gaze, later restricts upward gaze
and ultimately may result in paralysis of all eye movements; trouble swallowing (dysphagia);
cognitive dysfunction and a prominent gait disorder (gait apraxia and rigidity) with early falls.
Other signs and symptoms are: a syndrome known as “pseudobulbar palsy” which consists of
(pathological crying without feelings of sadness, masked facies and dysarthric speech); reduced
spontaneous blinking; abnormal stiffening and extension of the neck known as a retrocollis and a
wide-eyed stare with raised eyebrows which gives rise to a facial expression of surprise. The
“applause sign” (the patient can’t clap hands together three times only, as a result, the patient
often claps many more than three times) is likely present and can be helpful in distinguishing
PSP from Parkinson’s Disease and Frontotemporal Dementia. Neuroimaging of PSP patients
shows: atrophy of the midbrain with cisternal and ventricular dilatation and thinning of the
quadrigeminal plate.
The cognitive dysfunction and personality change seen in patients with PSP are generally milder
in degree than those seen in patients with primary dementing illnesses such as Alzheimer
disease. The cognitive dysfunction includes apathy, impaired verbal fluency, frontal release
signs, echopraxia or echolalia and impaired abstract reasoning. The disease usually develops
after age 40 and before age 60, and the diagnosis is purely clinical.
In the very recent past, most sources suggested an average survival rate, following the onset of
symptoms, of 5 years with patients dying from medical conditions related to PSP such as
pneumonia. But now that the diagnosis appears to be made earlier based on vaguer symptoms
such as fatigue, headaches, arthralgias, dizziness, parkinsonism and gait problems with falls and
no evidence of other diseases that can explain these clinical features, it is thought that many
patients can live for 15 years after the diagnosis. Misdiagnosis is a potential pitfall with these
newer more flexible diagnostic criteria, however.
Recommendations: No medication is effective in halting the progression of PSP; however,
medications that may provide modest symptomatic improvements include dopamine agonists and
tricyclic antidepressants. Only a few patients respond to anticholinergic drugs and the responses
are often short-lived and incomplete. The combination of carbidopa and levodopa generally
produces no dramatic symptomatic improvement in patients with PSP. Treatment is pretty much
limited to things such as the use of weighted walking aids to reduce the number of falls and
prism glasses to compensate for supranuclear ophthalmoplegia. I understand she will be
discharged soon and treatment will revert to her neurologist at Xxxx Neurology.
___________________________
Drew Chenelly, Psy.D.
Clinical Neuropsychologist This document was created using voice recognition software.