Endocrinological disorders of the nervous system

From the nervous system (hypothalamus, pituitary) --> focal, subacute or chronic

From the endocrine (thyroid, parathyroid, etc.) --> diffuse, subacute or chronic

From the vasculature --> diffuse or multi-focal, acute to chronic

• 1. Diabetic polyneuropathy
• -most common cause in western world
• -symmetrical, distal, small fiber polyneuropathy (long subacute or chronic)
• -Axonal injury with occasional segmental demyelination
• -Sensory> motor. Presents with dysesthesia, pareshtesias, frank allodynia and neuropathic pain

50% of diabetics have clinical polyneuropathy at 25 years post dx

• 2. Diabetic mononeuropathy
• -sudden onset dysfunction of peripheral nerve
• -most common: "Diabetic third nerve palsy" - sudden onset painful lesion of CNIII - spares pupillary function
• -most cases there is slow improvement over weeks to months

• 3. Diabetic --> ischemic stroke
• -Risk of atherothrombotic, lacunar, and embolic stroke increased due to: atherosclerosis, arteriolosclerosis, and coronary artery disease
• 4. Diabetic retinopathy
• -progressive loss of visual acuity, restriction of visual fields
• -microangiopathic changes. Ischemia results in microhemorrhages
• -retinal angiogenesis and neovascularization

• 5. "Diabetic encephalopathy"
• -delirium, lethargy/stupor/coma

• Evaluation/Tx:
• -Screen for DM: HbA1c, fasting blood sugar
• -Screen for neurological complications: ophthalmologic screens, food tacre
• -rule out other potential causes
• Tx:
• -control sugars
• -education
• -Pain meds for neuropathic pain (tricyclics, duloxetine, gabapentin, pregabalin

Hypermetabolic state (due to increased thyroid hormone, increased activity of sympathetic nervous system)

Sx: widened palpebral fissure, tremor or chorea, proximal myopathy, atrophy and weakness, anxiety, insomnia, emotional lability, irritability, inability to concentrate, anxiety, hyperactivity

• 85% is due to Graves' disease
• -Pts have "ophthalmopathy" - hypertrophy of retro-orbital tissues including the musculature, which leads to proptosis and ophthalmoplegia

Subacute onset

• Infants/small children = "cretinism",
• -Presentation: impaired CNS development with mental retardation that can be severe

• Older children/adults = "myxedema", or hypothyroidism
• -Presentation: slowing of mental and physical function, fatigue, apathy, sluggishness, myopathy, ataxia (truncal > appendicular), distal polyneuropathy, carpal tunnel syndrome
• -severe condition can lead to comatose
• -Do not metabolize drugs well, particularly susceptible to CNS depressants

Subacute onset over weeks to months

Evaluation:  TSH

Tx:  suppression or replacement of hormone

• - Cushingoid habitus: central obesity, moon facies, abdominal striae
•     - subacute onset over months

• - Behavioral changes: mild euphoria, energetic, irritability and insomnia, ...all the way to frank mania and psychosis
•     - onset over days

• -proximal muscle weakness and atrophy
•      - develops over months

• Causes: iatrogenic, endogenous source (ACTH-secreting pituitary adenoma = Cushing's disease)
• -short course of low dose glucocorticoids are unlikely to result in clinical dysfunction
• -high dose or chronic glucocorticoid are likely to result in clinical changes

• Pathology: 
• -brain: limited to pituitary gland
• -muscle: pathology differs between acute and more chronic clinical phenotypes

Pt with Guillain Barre should never be given high dose steroids

Abnormal secretion of growth hormone that begins after the closure of the bony epiphyses.

Presentation: there is enlargement of soft tissues and of the bones of the hands, face, and feet

Causes: pituitary adenoma (active)

Neuro complications: carpal tunnel syndromes or other focal nerve entrapments.

Growth hormone secretion prior to epiphyses closure, leads to gigantism