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51 Cards in this Set

  • Front
  • Back

When a thunderclap headache (TCH) is identified, what is the next step in management?

CT of the head, followed by lumbar puncture if the CT is negative; however, depending on the clinical picture, MRI of the brain with or without additional neurovascular imaging may be needed for diagnosis and management

Most common cause of thunderclap headache?

Subarachnoid hemorrhage (SAH) - 25%; initial evaluation of a TCH should focus on ruling out a subarahnoid hemorrhage

What are sentinel headaches?

Headaches that are clinically similar to SAH headaches, except they do not have neck stiffness, altered mental status, or focal neurologic symptoms. Likely due to a small undetectable leak instead of a structural change the aneurysm wall resulting in pain

Diagnostic value of CT in the setting of TCH

100% within the first 12 hours of symptom onset but decreases to 50% within 1 week

Most important diagnoses to consider in thunderclap headache? (9)

1. Subarachnoid hemorrhage (SAH) (20%)

2. Cervical artery dissection (20%)

3. Reversible cerebral vasoconstriction syndrome

4. Posterior reversible encephalopathy syndrome

5. Cerebral venous sinus thrombosis

6. Spontaneous intracranial hypotension

7. Stroke

8. Pituitary apoplexy

9. Third ventricle colloid cyst

Clinically, how do patients with a cervical artery dissection present? (5)

1. Headache that is ipsilateral to the dissection

2. Usually located in the jaw, face, ear, and periorbital and frontal regions

3. Localized to the occipital region

4. Nonthrobbing and severe pain

5. Unilateral Horner syndrome can often be seen

How is the diagnosis of reversible cerebral vasoconstriction syndrome made?

By the presence of diffuse, segmental cerebral vasoconstriction seen on MRI coupled with MRA of the head

Imaging and angiographic findings with RCVS may be indistinguishable from its main differential diagnosis, which is?

Primary angiitis of the central nervous system (PACNS)

Difference between RCVS and PACNS?

RCVS - thunderclap onset

PACNS - subacute, gradually progressive onset

Mainstay treatment of RCVS

Calcium channel blockers

Mainstay treatment for PACNS


Prognosis for RCVS

favorable with prompt diagnosis and management, although diagnostic delay can result in permanent neurologic sequelea

Complications of RCVS


Ischemic and hemorrhagic infarctions

Posterior reversible encephalopathy syndrome (PRES)-like changes on MRI

Prognosis of PACNS

Poor; even with prompt diagnosis and management, permanent neurologic deficits are common

Clinical features of posterior reversible encephalopathy syndrome

Global and focal neurologic syndromes and signs, such as altered mental status, visual loss, and seizures. May present with TCH.

How is the diagnosis of posterior reversible encephalopathy syndrome made? (3)

1. MRI of the brain shows vasogenic edema most often in the posterior white matter and cortex, although more frontal areas can be involved.

2. CT of the head and subsequent lumbar puncture will miss the diagnosis!

3. PRES can occur in patients who present initially with RCVS, and vice versa. Identifying RCVS with PRES is important because its presence will change management

Treatment of PRES

1. Depends on the underlying cause: acute hypertensive crisis requires a graduated decrease in blood pressure.

2. If PRES is due to eclampsia, magnesium is commonly used

3. RCVS in association with PRES may require CCBs in addition to other measures to lower the BP without causing hypoperfusion in the presence of stenoses

Up to ___% of patients with cerebral venous sinus thrombosis (CST) present with a TCH without other neurologic signs


Clinical features of CVST headaches

1. Persistent

2. Progressive

3. Exacerbated by Valsalva maneuvers, such as couging, heavy lifting, or bearing down

4. Lying down also increases ICP and can be prainful for these patients

Most striking characteristic of a spontaneous intracranial hypotension headache

Postural aggravation

Features of spontaneous intracranial hypotension

1. Postural aggravation, orthostatic headache resolves with recumbency

2. Young or history of minor trauma or connective tissue disorder

3. Bilateral

4. Additional neurologic symptoms are often present

MRI findings in spontaneous intracranial hypotension

1. Diffuse pachymeningeal enhancement and extradural fluid collections

2. "Brain sag" with low-lying cerebellar tonsils

3. Crowding of the psoterior fossa

4. Subdural hematomas

5. Effacement of the prepontine cistern and flattening of the pons

6. Descent of the optic chiasm

Best test for identifying a leak in spontaneous intracranial hypotension?

CT myelogram

First-line treatment for spontaneous intracranial hypotension? If that fails?

Large-volume (20 mL) blind epidural autologous blood patch, which can be repeated 2 to 3 times if there is a partial response; if this fails, the site of the leak can be localized with a myelogram and terated with targeted epidural blood patches, fibrin glue injections, or, in refractory cases, neurosurgical intervention

Features of pituitary apoplexy (5)

1. Holocranial headache with an acute or thunderclap onset

2. Nausea and vomiting

3. Constriction of visual fields

4. Ophthalmoplegia

5. Systemic symptoms vary wildly (e.g., adrenal crisis and coma)

Trigeminal neuralgia is _______

the most common cranial neuralgia, with an incidence of 8 per 100,000 persos

Average age of onset of trigeminal neuralgia

50 years

Clinical features of trigeminal neuralgia

1. Unilateral, severe, stabbing, lancinating pain in the distribution of the trigeminal nerve

2. Lasting from seconds to 2 minutes

3. May be precipitated by mechanical factors

Underlying pathophysiology of trigeminal neuralgia?

Irritation of the trigeminal nerve, which is usually idiopathic; however, structural causes should be investigated

Surgical options to treat trigeminal neuralgia can be considered when medical options have been ineffective. What are the surgical options? (2)

1. Neuroablative procedures that include alcohol block, balloon compression, radiofrequency ablation, and Gamma Knife radiosurgery

2. Microvascular decompression (90% immediate relief; 3.5% recurrence rate annually)

Complications of microvascular decompression? (4)

1. Cranial nerve deficits

2. CSF leak

3. Hemorrhage

4. Anesthesia dolorosa (numbess with pain in the numbed area)

Clinical presentation of patients with geniculate neuralgia

1. Unilateral, lancinating pain within the ear that lasts for seconds to minutes

2. May occur several times a day

3. Can develop into a chronic, dull pain within the ear

Pathophysiology of geniculate neuralgia

Facial nerve irritation that is idiopathic or secondary to a structural lesion and MRI with and without contrast should be performed

Characteristics of glossopharyngeal neuralgia

Severe, lancinating pain the throat and at the base of the tongue that can radiate to the ear; treated and diagnosed with nerve blocks

Incidence of idiopathic intracrnial hypertension (pseudotumor cerebri)

1-2 per 100,000 worldwide

Underlying pathomechanism of IIH?

Controversial: the 2 leading hypotehses are increased brain water content or increased resistance to CSF outflow (or both). The mechanism for headache is either cerebral venous distention or meningeal irritation from increased CSF pressure

Clinical presentation of IIH (3)

1. Acute to subacute onset

2. Constant pain, worse with recumbency and exacerbated by Valsalva maneuvers

3. Commonly retro-ocular pain is reported and transient visual obscurations provoked by postural changes occur in 50% to 75% of patients

Criteria for diagnosis of IIH (3)

1. Normal MRI

2. Normal CSF findings with pressure of 250 mm H2O or more

3. Typically, bilateral papilledema is considered necessary for diagnosis

Treatment of IIH? (4)

1. First-line treatment is acetazolamide in doses of up to 4 g daily

2. Therapeutic lumbar punctures can lower the ICP, but repeated taps are not ideal from a patient perspective and are not recommended because patient avoidance may result in visual loss from a lack of treatment

3. Neurosurgical intervention is indicated in rapidly progressive visual loss refractory to medical treatment

4. VP- or LP shunts are effective for reducing CSF pressures, and optic nerve sheath fenestration is used for relief of papilledema and stabilization of visual loss

Clinical presentation of giant cell arteritis (5)

1. Scalp tenderness

2. Jaw claudication

3. Polymyalgia rheumatica

4. Constitutional symptoms

5. Headache

Describe the headache pain in giant cell arteritis (2)

1. Usually constant and throbbing with associated scalp and temporal artery tenderness

2. Amaurosis fugax can occur and is a waning of permanent visual loss

Complications of giant cell arteritis?

1. Visual loss is end stage

2. Ischemic stroke due to involvement of the extracranial cervical vessels

How is the diagnosis of GCA made?

1. Clinical features, with determination of ESR or CRP (or both), and these should be considered for every elderly patient with new-onset headache

2. Biopsy documenting granulomatous arteritis

Treatment of GCA?

Corticosteroids, which can be tapered over 6 to 12 months

Occurrence of headache with neoplasms?

50% of patients with brain tumors have a headache

Pathophysiology of headache with brain tumors?

Likely increased ICP, impingement of dural structures, hydrocephalus, or a combination of all of these

Define Chiari Type I malformation (4)

Age dependent tonsillar descent below the level of the foramen magnum:

1. First decade of life, 6 mm below the foramen magnum

2. Second and third decades, 5 mm

3. Fourth through eight decades, 4 mm

4. Ninth decade, 3 mm

Underlying pathophysiology leading to head pain in Chiari Type I malformation?

Compression of neural tissues and the alteration in CSF dynamics

Clinical presentation of Chiari Type I malformation? (3)

1. Headache precipitated by Valsalva maneuver or cough

2. Localized occipitally

3. Brainstem compression may cause posterior fossa symptoms, including vertigo, ataxia, nystagmus, or hearing loss

Number of patients with OSAP that complain of headache?

50%; present upon wakening, and gets better through the day. Polysomnogram aids in the diagnosis of OSAP

Most common patient scenario for IIH?

Obese woman of childbearing age