Neurology Flashcards
Spinal Cord Compression - def? etiology?
An acute syndrome of back pain associated with compression of the spinal cord. It is considered a neurologic emergency.
- Commonly caused by cancer (lymphoma; multiple myeloma; carcinomas of prostate, lung, breast, kidney, or colon), herniated disk, epidural abscess, hematoma, or trauma.
- Acute cases are caused by trauma.
Spinal cord compression - clinical presentation?
Patients commonly present with insidious onset of mild sensory disturbance, lower extremity weakness, and/or sphincter or sexual dysfunction. Pain is the earliest symptom in the majority of patients (96%)
- The diagnosis of acute spinal cord compression has to be suspected on the basis of the history and neurologic exam.
- On neurologic exam, a dermatomal sensory level with bilateral lower extremity weakness, increased lower extremity muscle tone, and upper motor neuron signs below the level of compression are all consistent with the diagnosis of acute cord compression
- MC site is thoracic cord b/c narrowest
What is the Dx & Tx of spinal cord compression?
- can do xray but
- The diagnostic test of choice is an MRI of the spine. When MRI of the spine is contraindicated, CT myelogram is the diagnostic test of choice.
- High-dose dexamethasone should be started immediately once the diagnosis is suspected. After the specific etiology is delineated more clearly by MRI, specific therapy may be initiated.
- For radiosensitive tumors, such as lymphoma or multiple myeloma, radiation therapy should be started as soon as possible.
- Surgical decompression is the treatment of choice for a herniated disk, epidural abscess, or hematoma
What is the prognosis of pt w spinal cord compression?
The prognosis depends mainly on the functional status of the patient at the time of presentation.
- Up to 80% of patients who are initially able to ambulate retain that ability after treatment.
- Only 5% of patients without antigravity leg strength are able to ambulate after treatment.
Syringomyelia - etiology? 2 types? clinical presentation?
Syringomyelia is defined as cavitation of the spinal cord. It occurs as either communicating (with the CSF pathways) or noncommunicating.
- Communicating syringomyelia is usually associated with the congenital Arnold Chiari malformation
- noncommunicating syringomyelia is typically secondary to trauma or tumors of the spinal cord.
- clinically presents The loss of pain and temperature occurs in a cape-like distribution across the neck and arms. There is sparing of tactile sensation, position, and vibratory sense. Reflexes are lost.
- as the lesions enlarges there can be LMN signs at the level of the lesion with UMN below the lesion
- commonly occurs in the cervical cord level
What is the Dx & Tx of syringomyelia?
MRI most accurate
Treatment is surgery
Subacute combined degeneration - def? clinically signs? treatment?
- usually due to B12 def
- Patients will complain of distal paresthesias and weakness of the extremities followed by spastic paresis and ataxia. On exam there is a combined deficit of vibration and proprioception with pyramidal signs (plantar extension and hyperreflexia).
- Dx - established by finding lower B12 level
Tx - replace B12
Anterior spinal artery occlusion - clinical presentation?
Anterior spinal artery occlusion presents with acute onset of flaccid paralysis that evolves into a spastic paresis over days to weeks.
- Additionally, there is loss of pain and temperature sensation with sparing of vibration and position sense as the posterior columns are supplied by the posterior spinal artery.
- Everything (motor, sensory, autonomic) is lost below the level of the infarction with the striking exception of retained vibration and position sense.
- dorsal column remains untouched - everything else affected
Brown Sequard Syndrome - def? etiology
Hemisection of the cord results in a lesion of each of the 3 main neural systems: the principal upper motoneuron pathway of the corticospinal tract, one or both dorsal columns, and the spinothalamic tract.
- The hallmark of a lesion to these 3 long tracts is presentation with 2 ipsilateral signs and 1 contralateral sign.
Clinical presentation of Brown Seq Syndrome?
- lesion of CST - causes ipsilateral spastic paresis below the level of the injury
- lesion to fasciculus gracilis or cuneatus - causes ipsilateral loss of joint position sense, tactile discrimination & vibratory sensation below the lesion.
- lesion to STT causes contralateral loss of pain & temp starting 1 or 2 segments below the level of the lesion
- @ the level of the lesion - there is ipsilat loss ALL sensations including, touch, pain & temp, and ipsilateral flaccid paralysis of muscles supplied by injured cord segment
What is CVA - def? etiology?
A sudden onset of a focal neurologic deficit. Etiology includes several causes 1. large a. thrombosis 2. small a. thrombosis (lacunar) 3. embolic 4. vascular dissection 5. systemic HTN 6. bleeding
What is the clinical presentation of CVA?
Stroke should be considered in any patient who presents with acute onset of a focal neurologic deficit. The specific clinical syndrome is determined by the mechanism and vascular territory affected.
What are the 2 major systems that supply blood to brain?
- carotid - anterior circulation
2. vertebrobasiliar - posterior circulation
What are the major blood vessels that make up anterior circulation?
ACA & MCA
What are the signs of ACA?
- contralat weakness and sensory loss of the leg more than upper extremities
- urinary incontinence
- confusion
- behavorial disturbances
MCA occlusion causes what signs
- contralat hemiplegia
- contralat hemisensory loss
- homonymous hemianopsia w eyes deviated towards cortical lesion
- dominant hemisphere is associated w aphasia
what are the arteries composed of the posterior circulation?
PCA
Basilar artery
vertebral arteries
what does the posterior circulation supply?
cerebellum
brain stem
occipital lobe of cortex and pons
What are the posterior circulation syndromes?
Weber
Benedikt
Wallenberg
Occlusion of PCA signs?
- contralat homonymous hemisanopsia
- visual hallucinations
- agnosias
Penetrating branches of PCA lead to what circulation syndrome?
Weber - CN 3 palsy w contralat hemiplegia
Benedikt - CN 3 palsy w contralat ataxia or athetosis (slow, involuntary, writhing movements)
syndromes associated with basilar artery branches?
Paramedian branches - “lock in syndrome” quadriparesis w/ intacted vertical eye movements
Wallenberg syndrome - PICA - post inferior cerebellar artery - ipsilat facial sensory loss, contralat body sensory loss, vertigo, ataxia, dysarthria, dysphagia and Horners
what happens when cerebellar arteries are occluded?
vertigo
vomiting
nystagmus
ipsilateral limb ataxia
How do you Dx CVA? initial? most accurate?
initial - noncontrast CT scan of head to distinguish hemorrhagic or ischemic strokes
- usually neg in first 48 hrs after ischemia so
- most accurate is diffusion weighted MRI
What is the diagnostic workup for CVA after initial and most accurate tests?
look for the source - embolic
- ECHO - “bubble study” done to detect patent foramen ovale or cardiac defects
- carotid duplex
- 24 holter monitor
- inherited hypercoag
- EKG - in SAH you can see ischemia and inverted T waves
How do you manage CVA?
TpA should be initiated w/in 3 hr of symptom onset
Aspirin is started 24 hrs after Tpa
What is the contradictions to Tpa therapy?
Contraindications to the use of tissue plasminogen activator include
- stroke or serious head trauma within 3 months,
- hemorrhage (gastrointestinal or genitourinary) within 21 days
- surgery within 14 days,
- history of intracranial hemorrhage,
- BP >185/110 mm Hg,
- current use of anticoagulants,
- platelets 15 seconds)
If patient is allergic to aspirin - what is the alter for CVA?
if pt is allergic to aspirin or has recurrent CVA despite being on aspirin then give dipyridamole in addition to aspirin or just switch to clopidogrel alone
What is the treatment of SAH?
nimodipine
- early (w/in days!) surgical intervention to clip off the aneurysm or embolize the vessel with catheter should be done if candidate is good for surgery.
When is carotid endarterectomy recommended?
recommended when an occlusion exceeds 70% of the arterial lumen and the lesion is symptomatic.
- Endarterectomy may benefit those who are asymptom- atic if there is >60% stenosis in men age <60.
- The benefit of endoarterectomy is less certain in women because they have a lower risk of stroke.
- The more severe the disease, the greater the benefit. Carotid stenting is an alternative to endarterectomy.
What is the alternative to endarterectomy?
carotid stenting
When is carotid angioplasty and stenting not as good as endaterectomy?
ymptomatic patients with >70% stenosis.
- Angioplasty and stenting should be considered only for those who cannot undergo surgical endarterectomy.
What is the def of seizures?
A seizure is a paroxysmal event due to abnormally discharging central nervous system (CNS) neurons.
What is epilepsy?
Epilepsy is defined as a condition of recurrent seizures due to a chronic underlying process.
What is the etiology of seizures? VITAMINS
Vascular (stroke, bleed, arteriovenous malformation) Infection (meningitis, abscess, encephalitis)
Trauma (especially penetrating)
Autoimmune (CNS vasculitis)
Metabolic (hyponatremia, hypocalcemia, hypomagnesemia, hypoglycemia, hypoxia, drug overdose/withdrawal)
Idiopathic
Neoplasm
pSychiatric
What is the clinical presentation of seizures?
A seizure is essentially a paroxysmal, involuntary event (associated with abnormal movement or change of consciousness or both).
- Characteristically, seizures are sudden in onset, with or without an aura.
- Patients often complain of disorientation, sleepiness, and aching muscles for minutes to hours after the event.
- Patients may also experience incontinence, tongue biting, and headache as a result of the seizure. It may be difficult at times to differentiate a seizure from syncope, and it is important to obtain a complete history from any individual who witnessed the event.
- Generally, patients with syncope will not complain of significant postictal symptoms. They will recover consciousness within several minutes of the event, and on physical exam will not have evidence of incontinence or tongue biting
What are the 2 types of classifications for seizures?
Partial vs. Generalized
complex vs. simple
What is partial seizure? what is simple partial and complex partial seizures?
Partial seizures occur within discrete portions of the brain. The patient will often complain of involuntary jerking of a finger or hand.
- When consciousness is maintained for the duration of the seizure, the seizure is termed a simple partial seizure.
- When there is a change in consciousness during the seizure, the seizure is termed a complex partial seizure.
What is it called when partial seizure progresses to generalized seizures? What does it mean?
When a partial seizure progresses to a generalized seizure, it is called a partial seizure with secondary generalization. Typically, the seizure will begin focally and become generalized as the seizure activity involves both cerebral hemispheres.
What is generalized seizures? what are some types?
Generalized seizures arise from both cerebral hemispheres spontaneously without any detectable focal onset.
- Generalized tonic-clonic (grand mal) seizures are characterized by tonic contraction of muscles throughout the body followed by intermittent relaxation of various muscle groups (clonic phase).
- Absence seizures (petit mal) are more common in children than adults; they are characterized by sudden, brief loss of consciousness without loss of postural tone.
- Atonic seizures are characterized by sudden loss of postural tone lasting 1 to 2 seconds.
- Myoclonic seizures are characterized by sudden, brief muscle contraction.
What is status epilepticus?
Status epilepticus is defined as recurrent or continuous seizures (lasting at least 5–30 min).
What is the Dx for epilepsy?
EEG is the test of choice for the diagnosis of epilepsy. The diagnosis of idiopathic seizures is made only after secondary precipitating factors have been ruled out. An abnormal EEG alone is not diagnostic of epilepsy.
- Always check serum electrolytes, glucose, toxicology, and arterial blood gas to rule out hypoxia as a cause of a patient’s seizure. CT scan or MRI of the head is usually indi- cated to rule out a structural lesion as the cause of seizure
What is the treatment of seizures?
The treatment of seizures can be divided into the acute management of the acutely seizing patient (status epilepticus) and the chronic management of the epileptic patient.
- 1st step is ABC (airway, breathing, circulation)
- evaluate and treat any precipitating causes of seizure. If a reversible cause is identified, treat aggressively. If the patient continues to seize, the following strategy is appropriate.
- initial drug of choice is lorazepam or diazepam, these medications work by potentiating GABA receptor function.
- If the patient continues to seize, add phenytoin or fosphenytoin, which inhibits sodium-dependent action potentials. CNS side effects of phenytoin include diplopia, dizziness, and ataxia. Systemic side effects include gum hyperplasia, lymphadenopathy, hirsutism, and rash.
- If the patient continues to seize add phenobarbital. Side effects include sedation, ataxia, and rash.
- If, despite all of the above therapy, the patient continues to seize, add midazolam or propofol.
Do you give long term drugs to first time seizure patients?
In patients with first-time seizure, anticonvulsant therapy should be started only if the patient has an abnormal neurologic exam, presented with status epilepticus, has a strong family history of seizure, or has an abnormal EEG
Treatment for generalized tonic-clonic seizures?
VA phenytoin lamotrigine - decreases glutamate releases, side effects are SJS carbamazepine levetiracetam
Treatment for absence seizures?
Ethosuximide - first choice
VA
Myotonic and atonic seizures?
VA - first choice
Partial seizures (complex and simple) treated with?
Carbamazepine & phenytoin - first line
VA & Lamotrigine - alternatives or levetiracetam
What do you stop seizure treatement?
It is very difficult to determine when to stop therapy. Therapy may be stopped if the patient has been free of seizures for 2–3 years. Sleep-deprivation EEG may be done first to determine if the patient is at low risk of a recurrence. A normal sleep- deprivation EEG means there is a lower likelihood of seizures.
What is vertigo?
Vertigo is defined as a false sensation of movement, i.e., the sensation of movement in the absence of actual movement.
What is the etiology of vertigo?
Vertigo may be caused by Ménière disease, labyrinthitis, positional vertigo, traumatic vertigo, perilymphatic fistula, and cervical vertigo.
- Other causes include vascular disease of the brain stem, arteriovenous malformations, brain tumor, multiple sclerosis, drug overdose, and vertebrobasilar migraine.
What is the clinical presentation of vertigo?
Patients who experience vertigo will describe a sensation of movement without actually moving. Commonly, patients will describe their environment spinning around them.
- Once you are convinced by the history that the patient is indeed experiencing an episode of vertigo, the next diagnostic question you have to answer is whether the vertigo is secondary to peripheral or central vestibular disease.
- Central vertigo - gradual onset, no tinnitus or hearing loss, vertical nystagmus, multidirectional, presence of neighborhood signs - diplopia, cortical blindness, dysarthria, ext weakness, numbness
- Peripheral vertigo - sudden, tinnitus or hearing loss is present, no neighborhood signs, horizontal nystagmus
What is the clinical signs of Meniere’s disease? Etio?
Ménière disease is characterized by tinnitus, hearing loss, and episodic vertigo. Each episode lasts 1 to 8 hours. The symptoms wax and wane as the endolymphatic pressure rises and falls. The two most common causes of Ménière disease are syphilis and head trauma.
What is BPPV? etiology?
Benign paroxysmal positional vertigo is a cause of peripheral vertigo that characteristically is exacerbated by head movement or change in head position.
- Typically, episodes will occur in clusters that persist for several days.
- There will be a latency of several seconds after head movement before the onset of vertigo. The vertigo usually lasts 10 to 60 seconds.
What is labyrinithitis? Etio?
Labyrinthitis presents with sudden onset of severe vertigo that lasts for several days with hearing loss and tinnitus. The disease frequently follows an upper respiratory tract infection.
What is perilymphatic fistula?
Perilymphatic fistula is a form of peripheral vertigo related temporally to head trauma (blunt trauma to the ear, e.g., a slap to the ear) or extreme barotrauma during air flight, scuba diving, or vigorous Valsalva maneuver. Explosions deafen people.
How is central vertigo caused?
Central vertigo is caused by any cerebellar or brain-stem tumor, bleed, or ischemia. Drug toxicity or overdoses are important causes of central vertigo. Also, in the young patient with unexplained central vertigo, consider multiple sclerosis.
What is the treatment of peripheral vertigo?
Symptomatic treatment for peripheral vertigo includes meclizine or, in severe cases, diazepam.
What is the treatment for Meniere disease?
Ménière disease is treated with a low-salt diet and diuretics. In patients who fail medical therapy, you can consider surgical decompression.
What is the treatment for BPPV?
Benign paroxysmal positional vertigo is treated with positional maneuvers that attempt to move the otolith out of the circular canals (e.g., Dix Hallpike and Barany maneuvers).
