Miscellaneous clinical pain & neuroanatomy

Miscellaneous clinical notes space-chronic pain

*Allodynia to cold is an indicator of central sensitization

*Patient's especially sensitive to cold are more likely to be sympathetically maintained

*Cord injury,

CRPS space-four criteria for diagnosis

#1. In inciting event

#2. Pain out of proportion

#3. Vasomotor autonomic phenomenon

#4. Lack of an alternative explanation for the pain

*This is a controversial topic because of disability implications of this diagnosis

Three drugs with NMDA receptor antagonism

Amantadine

Dextromethorphan

Methadone

Treating migraine in a pregnant patient

Thorazine or magnesium

Treatment of chronic pain

#1  cool water, compounded cream consisting of ketamine and amitriptyline

#2 anti-inflammatory agents, antidepressants and antiepileptic agents

-Antidepressants good for neuropathic pain, and epileptic prescription for neuralgic patients

#3 dorsal cord stimulators peripheral nerve stimulator is

#4 intrathecal pump

#5 motor cortex and deep brain stimulator implantation

#6 destructive procedures although not currently recommended and is only recommended for terminal patients because of major complication anesthesia dolorosa which has no known treatment

Localization in clinical neurology of Paul Brazis textbook notes

Weber syndrome - third nerve palsy with contralateral hemiparesis lesion at the crus cerebri

The descending corticospinal tract has ~1million fibers on a side, only 3% originate from Betz cells (layer V in the primary motor cortex)

*Cortical spinal neurons also arise from postcentral gyrus and a somatosensory cortex, lateral prefrontal supplemental motor and cingulate gyrus as well

eponym for the pyramidal decussation -Mistichelli crossing - anywhere between 75-90%.

Cortical spinal fibers that descend ipsilaterally do so in Turcks bundle otherwise known as the anterior

corticospinal tract - although most of these will eventually decussate as well only 2% at the end remained

ipsilateral innervating axial musculature

Corticobulbar pathway- descends in the genu of the internal capsule

The ventral aspect of the facial nucleus innervating the lower two thirds has a crossed supranuclear input

Emotional facial movements do not descend via the internal capsule, the right cerebral hemisphere is dominant for facial expression or motion

Three direct pathways of cortical input to the basal ganglia

#1 internal capsule

#2 external capsule

#3 subcallosal fasciculus

Indirect pathways for cortical input to the basal ganglia

cortical thalamic striate pathway

Cortical olivary pathway

Cortical pontine pathway

Cortical association areas projected predominantly to the caudate nucleus

Sensorimotor cortical areas projected predominantly to the basal ganglia

The cortex also directly inputs the substantia nigra subthalamic nucleus and claustrum

Cortical thalamic pathway-descending feedback mechanism for ascending thalamco cortical fibers -also known as the thalamic radiations, also known as corticofugal pathway. descending mainly in the anterior limb of the internal capsule

Thalamic nuclei involved in cortical thalamic pathway feedback

anterior nucleus -> posterior cingulate gyrus

ventral lateral -> primary motor cortex

anterior ventral -> supplementary motor cortex

posterior -> sensory cortex

LGN -> primary visual cortex

MGN -> primary auditory cortex

Dorsomedial -> prefrontal cortex

Cortical hypothalamic tract

Multiple inputs to the hypothalamus (prefrontal cingulate amygdala olfactory hippocampus septal)

Alzheimer's disease quick numbers and facts to have on hand

Alzheimer's seminar notes

dementia has several features

impairment in daily life that is clinically significant

dyspraxia - inability to do rehearsed motor function

ideomotor - small well rehearsed motor tasks

ideation - dressing/writing

agnosia - 50% of cases unaware of their own dementia

decreased executive function

Alzheimer's path comes in two stages

insidious amyloid beta aggregation (can begin ~10.5 years prior to symptoms presentation)
  Keep in mind of 30% of the population has amyloid burden without any clinical indicators of dementia

Tau hyperphosphorylation w/tangles

Course of the disease includes pathological tissue aggregations well before clinical impairment is seen

1. Medial temporal/entorhinal cortex first to be affected

2. Cingulate

3. Neocortex

i.e. - memory, then limbic, then higher cognitive function

Alzheimer prevalence

5 million Americans, 26 million worldwide

Age 65-74 - 3-5%

Age 75-84 - 15%

Age 85+ - 45%

Risk factors

1. age most robust risk factor

2. female - (could be result of survival bias, women outlive men)

3. genetics (minor), APP, presenilin 1-2, APO-e4

Diabetes and smoking? Odd's ratio of getting Alzheimer's increased to 18-20!!

Anaplastic astrocytoma neuropath notes

Anaplastic, WHOIII, infiltrating aggressive, normally in cerebral hemispheres
-nuclear atypia, mitoses, high proliferation,
-mean age 45-50,
-Genetics (high tp53 mutation)
-mean time to transition to gbm ~2yrs, EGFr mutations have worse prognosis

Glioblastoma
-most frequent, most malignant brain tumor, WHO IV, can arise de novo or as malignant transformation, very invasive and cannot be fully resected, peak incidence 45-75.
-tumor most likely to be in cerebral hemispheres. however basal ganglia, thalamus, brainstem not uncommon, but see more in children.
-tumor very commonly spreads through corpus callosum, butterfly appearance on imaging
-imaging: ring enhancing, significant edema,
-GBM does not usually go to subarachnoid and so does not show up in CSF, hematogenous spread does not happen (very rare).
- multifocal GBM -true incidence unknown, estimated to be 2.4% of GBM to be multifocal

medicine clincial notes from 3rd year medical school recently discovered

low complement in renal disease suggests immune complex mediated pathology

when assessing complement levels, it helps to have two time points to establish a trend

Henoch Schonlein Purpura - 1/2 of all cases preceded by URI, especially strep, or vaccination or insect bites. Renal biopsy stain IgA, C3, Fibrin

Palpable Purpura (100%)

Arthritis (43-75%)

Abdominal Pain (20-30%)

Renal (21-54%)

 

women w/MI present very atypically

stigmata of chronic infection- temporal wasting, thenar wasting, interossei wasting, adenopathy

pulmonary manifestations of RA -

pulmonary effusion, greatly decreased glucose

pulmonary nodules

airway manifestations

interstitial lung disease associated with RA (NSIP)

decreased glucose? infection or RA

studding of diaphragm on cxr? interstitial disease

honeycombing is an end stage process of interstitial lung disease

never order ACE for sarcoid, its not an informative test

differential for miliary pattern on cxr

tb

sarcoid

pcp

varicella

metastasis

Clinical consult notes

neuro consults clinical notes

A call to the emergency department to see a patient with intractable facial pain. The patient was a 60 something-year-old woman with a history of trigeminal neuralgia who has had multiple at least 10 neurosurgical procedures in the past 20 years for facial pain. Two years ago she had a motor cortex stimulator implanted and has been using an unknown setting to help control facial pain. She is also taking carbamazepine which has been partially therapeutic. Recently in the last two weeks she has noticed that the stimulator is not helping her pain and she has been having breakthrough episodes of recurrent lancinating sharp-like episodic paroxysmal facial pain. These last anywhere between 30 seconds to two minutes and come in intervals which have been more or less constant for the previous week she has had very little sleep or food as a result. Aside from the carbamazepine she takes oxycodone with limited therapeutic effect. In the last few days she was seen in clinic and multiple setting changes were made both increasing and decreasing the voltage as well as changing the signal firing pattern. We are now been consulted by the emergency department for recommendations for this intractable facial pain. On exam she was otherwise stable but she was teary and the right face was flushed full a little swollen. Every now and again she would wretch forward with outbursts of moaning in pain. There were no focal neurological deficits

The most important first step is to control the patient's pain for which there are a couple of options. First we could increase the dose of the opioid medication in hopes that this could somehow treat the pain. Emergency Department personnel had already tried this, but it was not working after a few hours. Their method was to use oxycodone oral, approximately 30% stronger than oral morphine. We recommended intravenous opioids particularly hydromorphone as far stronger than oxycodone. The patient also kept a log of which stimulator settings worked best to control her pain. The current setting was not the most optimal setting that she previously had found. We recommended altering the setting to a prior pattern which she did with limited therapeutic effect.  These combined interventions were responsive for the patient in this instance and she was able to discharge with a prescription for oral opioids converted to the strength of the intravenous dose for the next day until she had follow up with her specialist. Had this not worked I have seen case reports of fosphenytoin loading for acute pain. And had that not worked unfortunately the last resort is general anesthesia and admission for intractable pain. Luckily for this patient she experienced symptomatic relief with stronger dose opioids for breakthrough pain and was able to leave the emergency department and make her clinic visit the day after.