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Neuropathology 1 > Headache disorders (neuropathology) > Flashcards

Headache disorders (neuropathology) Flashcards

1
Q

Primary Headache?

A

headache & its associated features are from the disorder itself

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2
Q

Secondary Headache?

A

Caused by an exogenous disorder

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3
Q

Most common type of primary & secondary headache’s?

A

Primary: Tension
Secondary: Systemic infection

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4
Q

Migraine Epidemiology?

A
  • 2nd most common cause of primary headaches
  • 15% women
  • 6% of men
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5
Q

Migraine definition?

A
  • Benign recurring headache associated with a particular additional neurological signs & symptoms
  • typically accompanied by nausea/ vomiting
  • often associated with triggers
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6
Q

What is the key path of pain in migraine?

A
  • trigeminovascular input

meningeal vessels > trigemina ganglion > synapse on 2nd order neuron in TCC in brainstem > thalamus > cortex

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7
Q

What modulates the trigeminovascular nociceptive (pain) input?

A

midbrain nuclei
1. dorsal raphe nucleus
2. locus coeruleus
3. nucleus raphe Magnus

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8
Q

What seems to be the cause of migraines?

A

Problems with modulation of pain sensation from the trigeminal affects
-abnormal pain sensation related to vascular dilation/constriction

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9
Q

How do Triptans (ex. Sumatriptan) work on migraines?

A

-acts on 5-HT1 receptors
-5-HT1 R are important in the trigeminal nucleus/thalamus
- bind serotonin released in the synapse.
-Triptans block these receptors

-used acutely, early on as migraine develops

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10
Q

What is CGRP (calcitonin-gene-related peptide), where is it active, and what does it do?

A
  • peptide neurotransmitter
  • active at the trigeminal ganglion & vasoactive efferents
    -vasodilator - increases pain sensation when released
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11
Q

What can be used to counteract CGRP?

A

-monoclonal antibodies
-they bind and eliminate CGRP, thus, it cannot bind to its R, preventing headache

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12
Q

Primary neural dysfunction theory?

A
  • wave of “spreading depression” travels through the cortex and leads to activation of the trigeminal complex
  • leads to vascular-generated pain

Spreading depression:
- slowly travelling wave of neural excitability
-depression because after the wave spreads, the area is refractory

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13
Q

What is spreading depression linked to?

A
  • linked to neurological findings (aura, visual changes)
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14
Q

Etiology of migraines?

A

strong genetic component
- 70% have a 1st degree relative with migraine
-maybe VG calcium channels? (unknown)

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15
Q

Prodrome?

A

-symptoms that typically precede the migraine & aura
-includes:
light, sound, odour sensitivity
lethargy, fatigue
food cravings, thirst
neck discomfort
mood changes, brain fog

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16
Q

Migraine aura?

A

-occurs before or during the migraine
-55% DO NOT experience this
-includes:
visual field defects, tunnel vision, scotoma, parenthesis, limb heaviness, confusion, speech difficulties

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17
Q

Scotoma?

A

area of impaired vision with a flashing light border

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18
Q

Acephalgic migraine?

A

Migraine without headache
-just prodrome & aura

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19
Q

Common migraine?

A

migraine without aura

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20
Q

Classis migraine?

A

Migraine with aura

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21
Q

Complicated migraine?

A

has severe or persistent (reversible) sensorimotor deficits
-diplopia, vertigo, ataxia, altered level of consciousness
-hemiplegia, loss of vision

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22
Q

Tension headache definition?

A
  • chronic head-pain syndrome characterized by bilateral tight-sandlike discomfort

-pain builds slowly, fluctuates in severity & may persist for days

-may be episodic or chronic

23
Q

Pathophysiological of tension headache?

A

-increased muscle tension (no different than tension in migraine)?
-increased sensitivity to myofasial pain
-dysregulation of pain sensation in CNS

24
Q

Symptoms of tension headache (6)?

A

variable in duration, more constant in quality, & less severe

-pressing/tightening (nonpulsatinle)
-frontal-occipital location
-bilateral
-mild-moderate intensity
-not aggravated by physical activity

25
Trigeminal autonomic cephalalgies?
group of headache syndromes includes: - cluster headache - paroxysmal hemicrania - SUNCT = short lasting unilateral neuralgia-form headaches with conjunctival injection & tearing -SUNA (like above but autonomic symptoms) -intense & excruciating
26
Pathogensis of cluster headaches & TAC?
no clear theory, may be linked to: - hypothalamic/circadian circuits - vasodilation as a result of CNS dysregulation -vasodilation of carotid a may compress sympathetic fibers, resulting in a shirt towards parasympathetic activation
27
What type of headaches do patients tend to move during the attacks (pacing, rocking rubbing, become aggressive)?
Cluster headaches & TACS
28
What headaches are episodic? (tend to occur daily for a period and then headache free for a period of time)
Cluster headaches & TACS
29
What are secondary headaches associated with (2)?
- elevation in intracranial pressure - irritation of meninges
30
What brain structures can cause pain in secondary headaches and what nerve innervates them?
intracranial vessels, dura mater, meningeal arteries, dural sinus, falx cerebri, pial arteries - all innervated by CN V
31
3 major types of cerebral edema?
1. Vasogenic 2. Cytotoxic 3. Interstitial edema
32
Vasogenic Edema?
BBB disruption & increased vascular permeability -fluid shifts from intravascular compartment to the intercellular spaces of the brain and thus, no lymphatics to remove excess fluid
33
What causes localized and generalized vasogenic edema?
Localized: infection, cancer (adjacent to inflammation or neoplasm) Generalized: uncontrolled hypertension
34
Cytotoxic edema?
Increase in intracellular fluid secondary to neuronal, glial, or endothelial cell membrane injury -from generalized hypoxic/ischemic insult or metabolic damage (any cause of cell death)
35
Intersititial edema? cause?
-usually occurs around lateral ventricles -increased intraventricular pressure causes abnormal flow of fluid from intraventircular CSF across the ependymal lining to the periventricular white matter -mostly due to hydrocephalus & increased intracranial pressure
36
Consequences of cerebral edema (4)?
1. gyri flatten 2. Sulci narrow 3. ventricular cavities compressed (or expand if edema cause is interstitial - hydrocephalus) 4. Herniation can occur as brain expands
37
How much CSF is produced a day and at what rate?
120 mL 0.3 mL/min
38
Hydrocephalus? Cause?
- accumulation of excessive CSF within the ventricular system - due to impaired flow & resorption of CSF (most cases)
39
macrocephaly?
increase in head circumference due to hydrocephalus in babies before closure of cranial sutures
40
Hydrocephalus after cranial sutures close?
results in enlargement of ventricles & increased cranial pressure -can result in atrophy/ compression of surrounding brain tissue
41
Communicating vs non-communicating hydrocephalus?
COMMUNICATING: - enlargement of entire ventricular system NON-COMMUNICATING: -only a portion of the ventricular system is enlarged
42
Symptoms of raised inter cranial pressure/ hydrocephalus (6)?
1. slowing of mental capacity 2. headaches (more severe in morning) 3. Vomiting (more likely in morning) 4. Blurred vision (optic n atrophy due to papilledema) or double vision (CN6 palsy) 5. Difficulty walking (spasticity) 6. KIDS: Precocious puberty, stuned growth due to hypothalamic impairment
43
What is Normal Pressure Hydrocephalus & causes?
ventricular volume is increased but arachnoid volume is not - pressures on lumbar puncture are normal -intracranial pressure is increased CAUSED BY: tumours, infections, subarachnoid hemorrhage
44
Normal Pressure Hydrocephalus Epidemiology?
Relatively common but rare in those under 60 20/100,000 prevalence in general elderly population
45
Normal Pressure Hydrocephalus clinical features?
- Gradual progressive gait apraxia (magnetic feet) - urinary continence - dementia -bradyphrenia: slowness of thought, speech
46
Normal pressure hydrocephalus treatment?
- many patients improve after shunt is placed
47
Idiopathic intracranial hypertension?
- affects obese women of childbearing age - chronically elevated intracranial pressure leading to papilledema, which may lead to progressive optic atrophy & blindness papilledema: swelling of optic disc
48
Idiopathic intracranial hypertension epidemiology?
- 1/100,000 - 8-20 X increased risk in obese women
49
Idiopathic intracranial hypertension pathogenesis?
- problems with venous drainage especially transverse sinuses - rate of arterial flow is greater than venous outflow leading to increased pressure
50
Idiopathic intracranial hypertension signs & symptoms (4)?
1. typical headache 2. diplopia (double vision) 3. Tinnitus 4. Visual field defects
51
Idiopathic intracranial hypertension diagnosis & treatment?
Diagnosis: Lumbar puncture to determine pressure Treatment: acute emergency treatment for elevated ICP & weight loss
52
Subfalcine (cingulate) herniation?
- due to increased intracranial pressure - untilateral or asymmetric expansion of cerebral hemisphere that displaces the cingulate gyrus under the flax cerebri - can lead to compression of the anterior cerebral artery
53
Transterntorial (uncinate, medial temporal) herniation
-due to increased intracranial pressure -medial aspect of the temporal lobe is comprised against the free margin of the tentorium can lead to: - CN3 palsy - Hemiparesis: compression of the contralateral cerebral peduncle -Duret Hemorrhage: hemorrhagic lesions in midbrain & pons
54
Tonsillar herniation?
-displacement of cerebellular tonsils through the foramen magnum -acute = life-threatening - compression of brainstem -chronic = less severe

Neuropathology 1 (1 decks)

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