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Nervous System & Special Senses > Neuropathophysiology > Flashcards

Neuropathophysiology Flashcards

1
Q

What effect do organophosphates have on the nervous system?

A

Organophosphates cause toxicity by phos. a residue on AchE, inactivating it. The irreversible blocking of this enzyme causes Ach accumulation.

Can also lead to organophosphate induced delayed polyneuropathy (OPIDP) which is caused by killing of neurons in the CNS secondary to acute or chronic poisoning. Results in demyelination of longest and largest nerves first. Associated with paralysis (footdrop) and axonal degeneration. Delayed neuropathy may occur (peripheral numbness/tingling).

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2
Q

What nerves are effected first in organophosphate-induced delayed polyneuropathy?

A

Largest and longest

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3
Q 
Organophosphate poisoning (Anticholinesterase
poisoning)
A

Often due to organophosphates (eg, parathion) that irreversibly inhibit AChE. Organophosphates
commonly used as insecticides; poisoning usually seen in farmers.

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4
Q

What are the effects of AchE poisoning?

A

Muscarinic effects: DUMBBELSS (reversed by atropine)

Diarrhea
Urination
Miosis
Bronchospasm
Bradycardia
Emesis
Lacrimation
Sweating
Salivation

Nicotinic effects: neuromuscular effects

CNS effects: resp. depression, lethargy, seizures, coma

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5
Q

What would happen with an occlusion of the posterior cerebral artery?

A

Occlusion of the posterior cerebral artery will lead to ischemia within the occipital lobe. Patients present with contralateral hemianopia with macular sparing.

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6
Q

What is the accronym we used to remember brainstem blood supply?

A

PAP is Bad Ass

Lateral:
PCA- midbrain
AICA- pons
PICA- medulla

Medial:
Basilar- pons
Ass- ASA

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7
Q

What is the most common type of spine tumors?

A

Spinal metastases

They may not stay in the bone and can metastasize to the spinal cord and compress

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8
Q

What cancer is associated (7.5%) with spine metastases?

A

Tumors of the prostate

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9
Q

What are common features seen in patients with spinal metastases?

A

Pain and point tenderness. The pain is usually deep and aching, often occurs at night, and may wake the patient from sleep.

Extension of the tumor inside the spinal canal may result in motor and sensory weakness that may become permanent.

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10
Q

What is the most common subtype of Guillian Barre syndrome?

A

Acute Inflammatory Demyelinating Syndrome

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11
Q

What happens in Acute Inflammatory Demyelinating Syndrome?

A

Rapidly progressive limbs weakness that ascends following GI/upper respiratory infection.

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12
Q

What is the pathophysiology of G.B.S.?

A

GBS is an autoimmune condition that destroys Schwann cells via inflammation and demyelination of motor fibers, sensory fibers, peripheral nerves (including CN III-CN XII).

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13
Q

What does G.B.S. present with clinically?

A

Symmetric, ascending muscle weakness/paralysis & depressed/absent DTRs beginning in lower extremities.

Bilateral facial paralysis and respiratory failure common

May see ANS dysregulation (cardiac irregularities, hypertension, hypotension)

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14
Q

What is the common CSF finding with G.B.S.?

A

Albuminocytologic dissociation (INC CSF protein like albumin with normal white blood cell count)

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15
Q

What is the treatment for G.B.S.?

A
  1. Respiratory support is critical (the diaphragm is a muscle!)
  2. DMARDs, IVIG, or plasma exchange
  3. Steroids have no place here
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16
Q

What are two bugs that are associated with G.B.S.?

A

Campylobacter jejuni and Zika virus

GBS frequently occurs following inflammatory, bloody diarrhea due to CJ

Also may occur following URI

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17
Q

What pre-existing condition increases risk for G.B.S.?

A

An autoimmune condition

In patient scenario, they had Hashimoto thyroiditis

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18
Q

What are common things you can measure in CSF?

A

Protein and glucose levels, cell counts and differential, microscopic examination, and culture

Additional testing such as opening pressure, supernatant color, latex agglutination, and PCR

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19
Q

What does the CSF opening pressure give you information on (what are general characteristics we should look out for?)

A

In general, opening pressure of CSF tells us about intracranial pressure.

Where the meniscus equilibrates on the collection pole with fluctuate between 2 and 5mm of patient’s pulse and between 4 and 10 mm with respirations.

Straining increases opening pressure. Hyperventilating decreases opening pressure.

Normal opening pressures increase with age.

Intracranial hypotension = 60 mm H2O (eg. CSF leak from trauma or previous LP).

Opening pressures above 250 mm H2O are diagnostic of intracranial hypertension. Elevated intracranial pressures is present in many pathologic states including meningitis, intracranial hemorrhage, and tumors. Idiopathic intracranial hypertension is a condition most commonly seen in obese women during their childbearing years.

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20
Q

What is normal CSF supernatant color?

A

Crystal clear

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21
Q

What was some conditions are causes of colored CSF supernatant?

A

WBC and RBC can cause CSF to appear turbid (present in infectious or inflammatory conditions)

Xanthochromia is a yellow, orange, or pink discoloration of the CSF, most often caused by the lysis of RBCs resulting in hemoglobin breakdown to oxyhemoglobin, methemoglobin, and bilirubin.

Another reason for orange colored CSF = high carotenoid ingestion

Brown colored CSF = meningeal melanomatosis

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22
Q

What do you know about CSF cell count?

A

Under normal conditions, CSF contains low counts of WBC. Individuals with bacterial meningitis will have more WBC present than individuals with viral meningitis BUT in both, WBC levels are increased.

Elevate WBC counts may occur after a seizure, in intracerebral hemorrhage, with malignancy, and in a variety of inflammatory conditions

23
Q

In meningitis, what would you expect the CSF-to-serum glucose ratio to be?

A

Normal to low to marked decrease

24
Q

Why do we care about or use the CSF protein level?

A

CSF protein concentration is one of the most sensitive indicators of pathology within the CNS. Newborns usually have more than adults

25
Q

What are the indications for high CSF protein levels?

A

Elevated CSF protein is seen in infections, intracranial hemorrhages, multiple sclerosis, Guillain Barré syndrome, malignancies, some endocrine abnormalities, certain medication use, abscess, epilepsy, acute alcoholism, and neurosyphilis

26
Q

What are the indications for low CSF protein levels?

A

Low CSF protein levels can occur in conditions such as repeated lumbar puncture or a chronic leak, in which CSF is lost at a higher than normal rate. Low CSF protein levels also are seen in some children between the ages of six months and two years, in acute water intoxication, and in a minority of patients with idiopathic intracranial hypertension. CSF protein levels do not fall in hypoproteinemia.

27
Q

Is CSF glucose usually lower or higher than serum glucose levels?

A

Lower. Regardless of serum levels (even in hyperglycemia), CSF levels do not go above certain threshold.

28
Q

In CNS infections, what happens to CSF glucose levels?

A

Bacterial - lower

Viral - usually normal

29
Q

What are some reasons for hypoglycorrhachia (low glucose level in CSF)?

A

Chemical meningitis, inflammatory conditions, subarachnoid hemorrhage, and hypoglycemia also cause hypoglycorrhachia

30
Q

Is there a pathologic process that causes CSF glucose levels to be elevated?

A

No- only possible causes is having elevated blood glucose

31
Q

What is the leading cause of viral meningitis?

A

Enterovirus

32
Q

What is latex agglutination used for?

A

Latex agglutination (LA) allows rapid detection of bacterial antigens in CSF.

33
Q

What can PCR be used for in CSF cultures?

A

Viral meningitis (EBV, CMV, HSV type 1, enterovirus)

34
Q

What is the pathophysiology of multiple sclerosis (MS)?

A

Oligodendrocytes provide the myelin sheath for axons in the CNS. MS is an autoimmune demyelinating process that occurs in the CNS.

Autoimmune inflammation and demyelination of CNS (brain and spinal cord) with subsequent axonal damage

35
Q

What can MS present with?

A
  • Acute optic neuritis (painful unilateral visual loss associated with Marcus Gunn pupil)
    -Brain stem/cerebellar syndromes (eg, diplopia, ataxia, scanning speech, intention tremor,
    nystagmus/INO [bilateral > unilateral])
  • Pyramidal tract demyelination (eg, weakness, spasticity)
  • Spinal cord syndromes (eg, electric shock-like sensation along cervical spine on neck flexion,
    neurogenic bladder, paraparesis, sensory manifestations affecting the trunk or one or more
    extremity)

*relapsing and remitting is most common clinical course

36
Q

MS is more common in individuals who grow up farther or near the equator and with what levels of Vit D?

A

More common in individuals who grew up farther from equator and with low serum vitamin D levels.

37
Q

What are the lab findings of MS?

A

INC IgG level and myelin basic protein in CSF

Oligoclonal bands are diagnostic

MRI is gold standard

Periventricular plaques (areas of oligodendrocyte loss and reactive gliosis)

Multiple white matter lesions disseminated in space and time.

38
Q

How do you go about treating M.S.?

A

Stop relapses and halt/slow progression with disease-modifying therapies (eg, β-interferon,
glatiramer, natalizumab). Treat acute flares with IV steroids. Symptomatic treatment for
neurogenic bladder (catheterization, muscarinic antagonists), spasticity (baclofen, GABAB
receptor agonists), pain (TCAs, anticonvulsants).

39
Q

What is osmotic demyelination syndrome?

A

Also called central pontine myelinolysis. Massive axonal demyelination in pontine white matter
2° to rapid osmotic changes, most commonly iatrogenic correction of hyponatremia but also
rapid shifts of other osmolytes (eg, glucose). Acute paralysis, dysarthria, dysphagia, diplopia, loss of
consciousness.

Can cause “locked-in syndrome.”

Correcting serum Na+ too fast:

“From low to high, your pons will die” (osmotic demyelination syndrome)

“From high to low, your brains will blow” (cerebral edema/herniation)

40
Q

What are the two major types of Chiari malformation?

A

Chiari I: Caudal displacement of cerebellar tonsils into foramen magnum

Chiari II Herniation of the cerebellar vermis, brainstem (medulla), and IVth ventricle into foramen magnum. Leads to noncommunicating hydrocephalus. More severe than Chiari I. Usually associated with aqueductal stenosis, lumbosacral myelomeningocele (may present as paralysis/sensory loss at and below the level of the lesion).

This is congential!

41
Q

How does Chiari manifest?

A

Chiari I malformation will be asymptomatic in childhood, but manifest in adulthood with headaches (w/ exertion) and cerebellar symptoms. Association with spinal cavitations (eg. syringomyelia/syrinx-backup of CSF)

42
Q

What is a Dandy-Walker malformation?

A

Agenesis of cerebellar vermis leads cystic enlargement of 4th ventricle that fills the enlarged posterior fossa.

Associated with noncommunicating hydrocephalus, spina bifida.

43
Q

With syringomyelia (CSF filled cystic cavity within spinal cord). what area of the spinal cord are we most concerned with?

A 
Cystic cavity (syrinx) within central canal of spinal cord . Fibers crossing in anterior white commissure (spinothalamic tract) are typically damaged first. Results in a “cape like,” bilateral, symmetrical loss of pain and temperature sensation in upper extremities (fine
touch sensation is preserved).
44
Q

What is the cogwheel rigidity test?

A

The cogwheel rigidity test is where a tremor is superimposed on the hypertonia, making the movement irregular due to intermittent increase and reduction of tone. Used diagnostically for Parkinson’s disease.

45
Q

What primarily causes bilateral hemianopia?

A

Expansion of pituitary adenoma, compressing the optic chiasm

46
Q

What is the most common pituitary adenoma?

A

A prolactinoma

47
Q

How does a prolactinoma present?

A

Prolactinomas can cause symptoms secondary to the hormonal effects of excess PRL and to the space-occupying effects of the tumor itself.

  • Reproductive-aged females can present with menstrual disturbance and/or infertility. The usual menstrual aberration in these women is oligomenorrhea, amenorrhea, or the occurrence of irregular menstrual cycles. Occasionally, if the prolactinoma occurs in a person of younger age, delayed menarche can result.
  • Galactorrhea can be spontaneous or expressive (only upon squeezing of the nipples).
  • Other features of hypoestrogenism include vaginal dryness, dyspareunia, and a decline in bone mineral density (ie, osteopenia or osteoporosis). (Estrogen promotes PRL release).
  • Men with prolactinoma have 1 or more features of hypogonadism, which may include decreased libido, erectile dysfunction, or infertility
48
Q

What is the relationship between prolactin and dopamine + estrogen?

A

Production of prolactin is controlled by two main hormones: dopamine and estrogen. These hormones send a message to the pituitary gland primarily indicating whether to begin or cease the production of prolactin. Dopamine restrains the production of prolactin, while estrogen increases it

49
Q

How does breastfeeding affect a woman’s reproductive system?

A

It has long been recognized that women who breastfeed their children have a longer period of amenorrhea and infertility following delivery.

50
Q

What does hyper-PRL do to the release on GnRH?

A

Decreases it, leading to hypogonadism

51
Q

How does dopamine inhibit prolactin secretion?

A

By binding and activating dopamine D2-receptors in the pituitary.

52
Q

Why wouldn’t you want to give an antipsychotic or dopamine antagonist to someone with hyper-PRL?

A

Wouldn’t be able to turn the secretion off! Dopamine is antagonist of PRL secretion

53
Q

What are D1 dopamine receptors associated with?

A

Movement and psychiatric disorders

Nervous System & Special Senses (1 decks)

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