Here, we report a case of a complex patient with Cushing’s disease who presented with multiple FND symptoms including nonepileptic seizures, bilateral lower extremity paralysis, decreased finger flexion resulting in limited hand function, and stuttering. This case illustrates a rare psychiatric manifestation of CS presenting as multiple neurological complaints
I get the impression that the authors looked up a list of symptoms for Cushing's on wikipedia then declared any other symptoms the patient suffered from as FND.
What would be more useful and less sadistic is for the patient to be treated for CS, get their thyroid checked, and get any nutrient deficiencies fixed
then find out which symptoms still exist.
I don't normally stutter. But there have been occasions when I do when my thyroid is untreated or under-treated, and when I've been low in various nutrients, or when I'm so out of energy I can barely talk. I don't think this should imply that I have FND.
There is a relationship between cortisol levels and thyroid hormone levels, and thyroid issues affect the gut and nutrient absorption too - but this is rarely or never acknowledged by doctors.
the paper said:
decreased finger flexion resulting in limited hand function
So, someone has stiff fingers, and this is a symptom of FND? Medicine has gone mad.
My bold :
While the etiology of FND is unclear, it is often associated with a psychological stressor, and recent research has identified that patients with FND demonstrate abnormal stress response and have elevated stress biomarkers levels, including cortisol [13].
If anyone had to use a short sentence to describe CS it would be something like :
"CS is caused by patients having too much cortisol."
But the authors seem to be saying that CS may be caused by FND.
...
There are also mentions of the patient having hypokalemia (although I think it is mild) - and that can do unpleasant things to muscle function even when it is mild. One thing I didn't see in the paper is any reference to treating his low potassium and what effect that had on his muscle function. In fact, immediately after mentioning the low potassium they mention giving him a tranquiliser,
not potassium.
After receiving 2 mg lorazepam, he regained the ability to follow simple commands and to communicate, although with significant speech latency and hypoverbality.
Psychiatry was consulted because the patient endorsed suicidal ideation.
The patient was a 28-year-old man who was bed-bound and could hardly move his lower body. Feeling the way he did isn't surprising.
I wonder if the stuttering mentioned is anything to do with his muscle function problems - and, naturally, once psych got involved he was put on an anti-psychotic - and they can cause huge problems with movement.
This just stunned me - my bold:
One year prior to admission, the patient appeared to have progressive extremity weakness and could not control the lower extremities. The patient was diagnosed with Cushing’s disease in the outpatient setting but did not receive treatment due to concurrent onset and rapid worsening of psychiatric symptoms including depression with anhedonia, poor oral intake, memory impairment, and suicidal ideation resulting in a five-month admission to a med-psych hospital.
So, this poor man had Cushing's diagnosed a year before, which is known to cause symptoms that appear to be psychiatric, and he wasn't treated for the CS because he had psychiatric symptoms? !!!!!!
Given history obtained and physical appearance notable for central and facial adiposity, dorsal fat pad, striae, ecchymoses, and thinned skin, psychiatry advocated for workup of Cushing’s disease.An endocrinology consult guided further investigations.
Hallelujah! Finally!
The patient’s 24-hour urine cortisol level was extremely elevated to
1767.4 mcg/24 hr (normal: <50 mcg/24 hr), confirming a diagnosis of CS. In addition, serum cortisol values were elevated to 31.6 mcg/dL in the morning and 23.1 mcg/dL in the evening. Further workup revealed that plasma
ACTH level was also increased to 119 pg/mL (normal: 6-50 pg/mL). An
MRI of the sella turcica was ordered and showed a mm pituitary microadenoma concerning for an ACTH-secreting tumor (Figure
1), resulting in a diagnosis of Cushing’s disease.
After treatment for his CS his symptoms started reducing and disappearing.
Psychology, physical therapy, and occupational therapy were also involved. The patient regained hand function, including the ability to eat independently and to write using a pen. Furthermore, after being bedbound for eight months, the patient was once again able to stand up and take steps with assistance. Depressed mood, anhedonia, and suicidal ideation decreased as the patient’s functional symptoms improved.
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I am amazed that anyone published this case study. It is indicative of a total failure of the medical profession that almost paralysed a young man for a year. The authors should be embarrassed to publish this.
The only benefit to publishing this is it gives information to the medical profession on what symptoms they might see in neglected CS.