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NEURO - Coggle Diagram

- - - - an acute hemorrhage with accumulation of blood between the skull and the dura, usually due to tearing of the middle meningeal vessels
      - lentiform shape, cannot cross suture lines
      - management: craniotomy + evacuation
    - - between the dura and arachnoid mater, due to disruption of the bridging cortical veins
      - lunar shape, can cross suture lines
      - management: surgery
    - - spontaneous
        
        worst headache of your life "thunderclap headache"
        
        RF: smoking, family history
        
        management: STAT head CT, if negative STAT LP with cell count, STAT CTA, STAT 4-vessel angiogram, mannitol or hypertonic saline if coma or dilated pupils, Nimodipine, transcranial dopplers
        
        complications: hydrocephalus, SIADH, cerebral salt wasting, vasospasm, delayed cerebral ischemia, seizure, heart failure, death
      - traumatic
        
        usually a little subarachnoid blood
        
        management: BP <140, keep in ICU for 24hrs, no Nimodipine
        
        no complications; good outcome typically
- - - - multiple clinically distinct events affecting different parts of CNS separated in time (>1 month apart)
    - - confirmed objective evidence for a single attack typical for MS
      - solitary sclerosis (SS)
        
        imaging findings do not fulfill minimum MRI requirement for MS but are typical for MS
      - single attack MS (SAMS)
        
        fulfill minimum MRI requirement for MS
    - - 30% fulfill criteria for single attack MS in 5 year follow up
      - pre-RIS
        
        asymptomatic individuals presenting with lesions typical for MS but not fulfilling diagnostic criteria
    - - 80% of people with MS ultimately evolve to this phase
      - at least 1 year of gradual disability progression, independent of clinical relapses
      - primary progressive vs. secondary progressive
  - - - recrudescence of symptoms from prior MS relapse or lesion, usually in the setting of increased core body temperature
      - Uhthoff phenomenon
        
        reoccurence of a neurologic deficit from an earlier relapse in the setting of increased core body temperature, classically observed with exercise
- - - - causes: fungi>bacteria; Mycobacterium tuberculosis, Treponema pallidum, Coxiella burnetii, Brucella spp., Leptoospira spp., Francisella tularensis, Actinomyces spp., Ehrlichia chaffeensis, Anaplasma phagocytophilum
      - at least 4 weeks symptoms
      - insidious new headache with/without mild neck stiffness, low-grade fever, night sweats, focal neurological finding (cranial nerve palsies)
    - - immunocompromised, outbreaks, exposure history
      - management: increased ICP may require a shunt, corticosteroids, amphotericin, fluconazole, flucytosine, voriconazole
    - - primary amebic encephalitis, granulomatous amebic encephalitis, cerebral malaria
    - - <1 month: streptococcus agalactiae, E. coli, listeria monocytogenes
      - 1-23 months: S. agalactiae, E. coli, H. influenzae, streptococcus pneumoniae, neisseria meningitidis
      - 2-50 years: S. pneumoniae, N. meningitidis
      - >50 years: S. pneumoniae, N. meningitidis, L. monocytogenes, aerobic gram-negative bacilli
  - - - asymptomatic
      - early
      - symptomatic
      - late
  - - - lateral columns --> spastic paraparesis (HTLV)
      - dorsal columns --> sensory ataxia (HIV, syphilis)
  - - - rapid course, ataxia, spasticity, combined with memory and cognitive deficits
    - - cannibalism
      - headache, aching limbs, ataxia, involuntary movements
    - - early ataxia and signs of corticospinal tract degeneration
- - - - negative: weakness, atrophy, exercise intolerance
      - positive: fasciculation, tremor, cramps
    - - negative: hypoesthesia
      - positive: paresthesias, allodynia, hyperalgesia, neuropathic pain
    - - negative: orthostatic hypotension, incontinence, erectile dysfunction, decreased sweating, gastroparesis
  - - - large fibers: diminished vibration/proprioception/fine touch
      - small fibers: diminished pin prick and temperature
  - - - diabetes
        
        most common cause of neuropathy worldwide
        
        treatment: glycemic control (most important), Duloxetine, Pregabalin, Capsaicin
      - nerve infarction
      - toxicity/metabolic
    - - Guillain-Barre Syndrome (GBS)
        
        men>women
        
        often follow URI or gastroenteritis by 10-14 days (CMV, mycoplasma, HIV, influenza A, EBV, H. influenza, enterovirus, C. jejuni)
        
        autoimmune demyelinating process secondary to molecular mimicry
        
        diagnostic criteria:
        
        progressive weakness in the legs and arms
        
        areflexia or hyporeflexia
        
        progression of symptoms lasting up to 4 weeks
        
        relative symmetry of weakness and sensory loss
        
        sensory symptoms and signs, if present, less impressive than weakness
        
        pain is common, often in the back and legs
        
        autonomic dysfunction common
        
        absence of fever
        
        albuminocytologic dissociation in the CSF by 3 weeks
        
        postgadolinium enhancement of peripheral nerve roots and cauda equina
        
        complication: respiratory failure
        
        variants:
        
        Acute Motor Axonal Neuropathy (AMAN) - more common in children, summertime, northern china
        
        Acute Motor-Sensory Axonal Neuropathy (AMSAN) - AMAN + sensory loss
        
        Miller Fisher Syndrome - ataxia, areflexia, ophthalmoparesis, generally have GQ1B antibodies
        
        Paraplegic form of GBS
        
        Pharyngeal-Cervical-Brachial Variant
        
        management: lumbar puncture (elevated protein + CSF cell count <10), admit to IMU/ICU if impending respiratory failure, monitor sodium closely, chemical & mechanical DVT prophylaxis, IVIG, plasma exchange
      - Charcot Marie Tooth (CMT)
      - Chronic Inflammatory Demyelinating Polyneuropathy (CIDP)
  - - - occurs with excessive use of hands
      - RF: pregnancy, obesity, RA, gout, DM, hypothyroidism, connective tissue disease, familial amyloid polyneuropathy, aromatase inhibitor use
      - management: conservative (splint, NSAIDs, steroid injections), surgery
      - females>males 3:1
    - - RF: post-op, critically ill patient, trauma, hematoma posterior thigh, prolonged sitting on a hard surface
      - weakness in knee flexion and weakness below the knee
    - - RF: post-op, critically ill, prolonged squatting, pneumatic compression, leg crossing
      - foot drop, toe extension, and foot eversion weakness, numbness of the lateral aspect of the leg, dorsum of the foot, and wedge between first and second toes
    - - ptosis and inferolateral displacement of the eye
      - RF: trauma, ischemia, orbital disease, cavernous sinus disease, aneurysm/mass compression, myasthenia gravis, ophthalmologic migraines
    - - aka "Tic douloureux"
      - paroxysmal stereotyped attacks of sharp stabbing pain in one or more divisions of the trigeminal nerve (more common in V2 and V3 divisions); episodes are rapid on onset, brief and self-resolving
      - triggers: chewing, talking, smiling, grimacing, brushing, washing the face, cold air
      - treatment: carbamazepine
    - - isolated seventh nerve palsy, deficits at presentation depend on where the lesion occurs
      - most cases are idiopathic
      - treatment: prednisone +/- antiviral
- - - - amnestic - memory is the affected cognitive domain; at-risk state for progressing to Alzheimer's disease
      - non-amnestic - deficit is not in memory domain
  - - - 60-80% of dementia cases
      - a disease of older age, unusual before age 65
      - early onset: 30-60s; often atypical features (less memory, more language, visual, or mood/behavioral changes at onset), more rapid progression
      - memory impairment (episodic particularly affected), executive functioning & judgement/problem-solving impaired, visuospatial impairments, language impairments, behavioral & psychological symptoms common
      - overall atrophy of brain, deposition of misfolded proteins, hyperphosphorylated Tau protein aggreated into clumps
      - RF: age, women>men, ApoE allele, hx of TBI, malnutrition/vitamin deficiencies, obesity, diabetes, CV dz/atherosclerosis, HTN, hyperlipidemia, smoking, alcohol, physical inactivity, low education level, metal toxicity
      - significant cognitive decline in at least one domain; interferes with independence in activities of daily living; loss of independent functioning
      - management: acetylcholinesterase inhibitors (Donepezil, Rivastigmine, Galantamine), NMDA receptor modulator (Memantine), Namzaric (combo pill)
    - - up to 20%
      - 5-10% of dementia cases show only vascular changes
      - any dementia that is primarily caused by cerebrovascular disease or impaired cerebral blood flow
      - two clinical scenarios:
        
        1) a clinically diagnosed stroke is followed by dementia
        
        2) brain imaging identifies vascular brain injury in a patient with dementia but without a clinical history of stroke
    - - 5% w/ LBD alone
      - progressive degenerative brain disorder characterized by dementia, psychosis, and features of parkinsonism (bradykinesia, resting tremor, rigidity)
      - core clinical features; fluctuating cognition with pronounced variations in attention and alertness, recurrent visual hallucinations that are typically well-formed & detailed, REM sleep behavior disorder
      - men>women
    - - up to 3.6% of dementia
      - 30-40% of PD have PDD
      - dementia that occurs in the context of well-established Parkinson's disease
    - - 2%
      - aka Pick's disease
      - gradual progressive decline in behavior, language or movement; marked by severe behavioral & personality changes often in the context of relatively preserved global cognition functioning; memory usually preserved
      - no cure, no medications slow or stop progression at this time
      - disinhibition, emotional blunting, changes in eating habits or diet, lack of insight, apathy, compulsive or ritualistic behaviors, deficits in executive function, other symptoms
    - - 50% of patients diagnosed with AD have pathological evidence of >1 cause of dementia
      - increased likelihood with increased age
- - - - location: anterior horn of the spinal cord, nerve roots, and peripheral nerves
      - damage from infections, GBS, hereditary neuropathies, compressive neuropathy, radiculopathy from intervertebral disk herniation, inflammation, or amyloid infiltration
    - - Amyotrophic Lateral Sclerosis (ALS)
    - - injury from stroke, MS, and spinal cord or brain masses
      - location: cerebral cortex, brainstem, and corticospinal tracts
  - - - autoimmune disease from antibodies blocking POST-synaptic ACh receptors
      - symptoms worse with exertion at the end of the day
      - proximal muscle weakness, neck weakness, double vision, droopy eyelid, trouble swallowing
      - management: acute - IVIG, plasma exchange; chronic - immunotherapy/immunosuppression, Mestinon, surgery (thymectomy)
    - - autoimmune disease from antibodies blocking PRE-synaptic voltage-gated calcium channels
      - improved strength with exercise
      - associated features: small-cell carcinoma, autoimmune conditions
      - weakness, diplopia, dysarthria, dysphagia, ptosis, shortness of breath, usually more predominant in LEs
  - - - vasculature: anterior cerebral artery, middle cerebral artery, posterior cerebral artery
      - signs: language difficulties, vision/gaze preference, cognition, behavior, personality, visual fields
    - - internal capsule
        
        dense hemiparesis
      - thalamus
        
        look for sensory symptoms plus decreased level of consciousness
      - brainstem
        
        symptoms can be bilateral
        
        diplopia, dysarthria, dysphagia, dizziness, vertigo, ataxia
        
        cranial nerve involvement
      - cerebellum
        
        incoordination, unsteadiness, imbalance, nystagmus, weakness
  - - - ipsilateral loss of proprioception and vibration, and motor paralysis/paresis
      - contralateral loss of pain/temperature
    - - "cape-like distribution" of weakness and numbness
      - UE>LE
      - +/- bowel/bladder symptoms
  - - - fasciculations, atrophy, can involve bulbar muscles
      - no sensory deficits
      - usually asymmetrical early & becomes symmetric in later stages
      - Amyotrophic Lateral Sclerosis (ALS)
        
        progressive loss of anterior horn cells
        
        UMN & LMN signs: progressive weakness and muscle atrophy, bulbar involvement (speaking/swallowing), no sensory symptoms, later on respiratory and bowel/bladder involvement
        
        sporadic or familial
        
        prognosis: death 2-4 years after onset
        
        management: Riluzole, Edaravone, supportive therapy (NIPPV, tracheostomy/PEG, anti-spasmodics, mood stabilizers, nutrition)
      - Primary Lateral Sclerosis
        
        more rare than ALS
        
        affects only UMN
        
        usually begins in the LEs with weakness & balance issues
        
        no significant muscle atrophy as in ALS
        
        symptoms: stiffness, weakness, spasticity, impaired balance, bulbar involvement
        
        prognosis: more slowly progressive compared to ALS & not as fatal
  - - - no sensory deficits
      - weakness, rarely pain, fatigue, soreness
      - Dystrophies
        
        genetic, progressive, degenerative muscle disorders
        
        Duchenne's
        
        mutation in the dystrophin gene
        
        3-5 years old with delayed motor milestones
        
        +Gower's maneuver
        
        wheelchair-bound by 12
        
        Becker's
        
        5-6 years old
        
        milder respiratory function
        
        learning disabilities more common
      - Inflammatory
        
        Dermatomyositis
        
        proximal>distal symmetric weakness, CK is normal or severely elevated, perimysial/perivascular inflammation, CD4 driven
        
        associated with: rash or skin manifestations, malignancy, vasculitis, connective tissue diseases, heliotrope rash, Gottron's papules
        
        management: immunosuppression (steroids)
        
        diagnosis: biopsy
        
        female>male
        
        Polymyositis
        
        female>male
        
        older patients
        
        proximal>distal symmetric weakness, CK is normal or severely elevated, endomysial inflammation, CD8 driven
        
        associated with: vasculitis, connective tissue diseases
        
        diagnosis: biopsy
        
        management: immunosuppression (steroids)
        
        Inclusion Body Myositis
        
        male>female
        
        older patients
        
        distal arm, proximal leg asymmetric weakness
        
        CK is normal or mildly elevated
        
        poor response to treatment
      - Metabolic
        
        occur from disorders of metabolism (glycogen, lipid, mitochondrial metabolism)
        
        Static
        
        proximal>distal weakness
        
        multi-organ involvement (cardiomyopathy, seizures, respiratory weakness)
        
        Dynamic
        
        changes with environment
        
        exercise, diet, cold exposure, anesthesia, infections
        
        rhabdomyolysis, pigmenturia, myalgia>cramps with endurance sports, shortness of breath with endurance sports, myalgia/cramps with power/sprint sports, symptoms triggered by fasting or superimposed illness, gout, nausea/vomiting with exercise, multiple system involvement
- - - - deterioration in neurologic deficits that occurs hours or days after initial presentation
    - - no further loss of neurologic function due to ischemia
    - - reemergence of previous stroke-related deficits in setting of physiologic stress (infections, metabolic derangements, etc.)
    - - [F]ace drooping
      - [A]rm weakness
      - [S]peech difficulty
      - [T]ime to call 911
    - - 1) acute management
        
        management: history, "Last seen/known normal/well" LNW, PMH, current medications, ABCs, manage/monitor blood pressure, NIHSS, blood glucose, non-contrast head CT, IV tPA*, endovascular therapy
      - 2) supportive care
      - 3) rehabilitation
        
        physical therapy, occupational therapy, speech therapy
      - 4) preventing recurrence
        
        varies depending on the etiology of the stroke
- - - - male>female 1.6:1; average age ~64
      - presenting symptoms: headaches, seizures, focal neurological deficits, AMS
      - treatment: maximum surgical resection, concurrent chemoradiation, chemotherapy [1st line = temozolamide (alkylating agent); bevacizumab (VEGF inhibitor)]
      - 46.6% malignant primary brain tumors
    - - ages 0-14
      - symptoms: headaches, cranial nerve palsies, ataxia, seizures
      - treatment: resection alone if operable, radiation & chemo if inoperable
    - - can treat with surgery alone
    - - treat with radiation & surgery; chemotherapy is optional
- - - - structural or metabolic abnormality
      - extracranial: sinusitis, otitis media, TMJ
      - intracranial: SAH, subdural hemorrhage, vascular dissection, sinus venous thrombosis, tumor, post-infection
      - metabolic disorders
      - post-traumatic headache
      - Temporal Arteritis
        
        headache developed in pts over 50 years old associated with jaw claudication, scalp tenderness, blurry vision
        
        treatment: high dose steroids
      - Idiopathic Intracranial Hypertension (IIH)
        
        symptoms of increased intracranial pressure: headache, blurry vision, double vision, vision loss, N/V
        
        typically seen in early adults, women, overweight or recent weight gain
        
        requires imaging and LP
        
        treatment: acetazolamide, optic nerve fenestration if vision is at risk
    - - no structural or metabolic abnormality
      - migraine type
        
        at least five attacks
        
        attacks lasting 4-72 hrs
        
        has at least two of the following characteristics: 1) unilateral location, 2) pulsating quality, 3) moderate or severe pain intensity 4) aggravation by or causing avoidance of routine physical activity
        
        during headache, experiences at least one of the following: 1) nausea and/or vomiting, 2) photophobia AND phonophobia
        
        not better accounted for by another diagnosis
        
        female>male; can be hereditary
        
        migraine with aura
        
        typical characteristics of migraine headaches + a gradual development of a mix of positive & negative features of aura, duration less than 1 hour with complete reversibility
        
        most common manifestation is visual changes; also nausea, fatigue, cognitive slowing; less commonly paresthesia, hemiparesis or hemiplegia, speech arrest
        
        triggers: exertion, dietary habits, sleep disturbances, head trauma/TBI, hormonal influences, medications, stress
        
        co-morbid conditions: mitral valve prolapse, Raynaud phenomenon, stroke, epilepsy, anxiety, depression, bipolar, social phobias
        
        treatments: acute abortive therapy (NSAIDs preferred, triptans), abortive therapy for prolonged migraines (triptan, IV antiemetic, IV toradol, IV Benadryl, Mg Sulfate, Valproic acid, IVMP), prophylaxis (propranolol, divalproex sodium, topiramate, amitriptyline)
      - tension type
        
        ill-defined syndrome and classified by frequency (infrequent episodic = 1 per month; frequent episodic = averaging 1-14 days per month; chronic = averaging more than 14 days per month)
        
        headache has at least two of the following pain characteristics: 1) bilateral location 2) mild or moderate intensity 3) pressing/tightening (nonpulsating) quality 4) no aggravation while climbing stairs or similar routine physical activity
        
        no nausea or vomiting, and no more than one of the photophobia and phonophobia
        
        most research suggest TTH is a multifactorial process involving both peripheral myofascial factors and CNS components
        
        triggers: mental or physical stressors, hunger, dehydration, overexertion, alterations in sleep patterns, caffeine withdrawal, female hormone fluctuations
        
        stress is a contributing factor
        
        treatment: regulation of sleep, meals and exercise, stress management techniques, passive physical manipulation and active cervical muscle stretching or exercise programs, behavior therapies, NSAIDs, caffeine, amitriptyline
      - cluster headache
        
        at least five attacks
        
        severe or very severe unilateral orbital, supraorbital, and/or temporal pain lasting 15 to 180 minutes
        
        headache is accompanied by at least one of the following: 1) ipsilateral conjunctival injection and/or lacrimation 2) ipsilateral nasal congestion and/or rhinorrhea 3) ipsilateral eyelid edema 4) ipsilateral forehead and facial sweating 5) ipsilateral miosis and/or ptosis 6) a sense of restlessness or agitation
        
        attacks have a frequency from every other day to 8 per day
        
        episodic: occurs in periods lasting 7 days to 1 year separated by pain-free periods lasting 1 month or more
        
        chronic: attacks occur for more than 1 year without remission or with remissions lasting less than 1 month
        
        treatment: oxygen, sumatriptan
      - trigeminal autonomic cephalgias (TAC)
        
        unilateral headache, usually stabbing pain and often retro-orbital
        
        prominent ipsilateral cranial autonomic features such as lacrimation, conjunctival injection or nasal symptoms
        
        types:
        
        cluster headache
        
        paroxysmal hemicrania
        
        short-lasting neuralgic HA with conjunctival irritation/injection (SUNCT)
        
        short-lasting neuralgic HA with autonomic features (SUNA)
      - chronic daily headache
        
        head pain for at least 4 hours for more than 15 days per month
        
        often develops from an episodic headache disorder either migraine or episodic tension type headache
        
        includes chronic tension type headache and chronic daily migraine
      - medication overuse headache (MOH)
        
        headache for 15 days/month with at least one of the following characteristics: 1) bilateral 2) pressing/tight non-pulsating quality 3) mild/moderate intensity
        
        simple analgesic use >15 days/month for 3 months
        
        headache has increased during analgesic use
        
        headache resolves or reverts to previous pattern within 2 months after discontinuation of analgesia
        
        treatment: wean pt off of the medication that is being overused, start prophylactic medication, give acute treatment, prednisone taper to break headache cycle, Botox treatment
  - - - subdural hemorrhage
      - subarachnoid hemorrhage
- - - - clinical triad: bradykinesia, resting tremor, rigidity, gait instability
      - non-motor symptoms: anosmia, constipation, REM sleep behavior disorder
      - decrease in dopaminergic neurons in the substantia nigra
      - sporadic disease due to abnormal alpha-synuclein containing Lewy Bodies
      - treatment: dopaminergic augmentation [dopamine agonists (bromocriptine, pramipexole, ropinirole), direct dopamine analogue (carbidopa-levadopa), MAOIs (selegeline, rasagiline), COMT-Is (entacapone, tolcapone)], deep brain stimulation
      - Plus Syndromes
        
        Multiple Systems Atrophy (MSA)
        
        synucleinopathy affecting oligodendroglia
        
        two subdivisions: cerebellar (20%) and Parkinsons (80%, previously Shy-Drager)
        
        prominent autonomic dysregulation; can also see spinal signs like spasticity and hyperreflexia
        
        Progressive Supranuclear Palsy (PSP)
        
        tauopathy
        
        high fall risk
        
        "stiff like a board", "Rocket sign", and inability to look upwards
        
        can have less striking autonomic features, oral-bulbar weakness that increases changes of pneumonia, sleep disturbance and impulsivity
        
        Lewy Body Dementia (LBD)
        
        synucleinopathy
        
        cognitive features occur prior to motor features, distinguishing this condition from Parkinson's disease
        
        prominent delusions and non-maleficent hallucinations
        
        Cortical Basal Syndrome/Degeneration (CBS/CBD)
        
        taupathy
        
        "Alien limb" phenomenon
        
        dementia is prominent as well as apraxia + parkinsonism, painful dystonias and myoclonus
  - - - due to triple repeat expansion on chromosome 4
      - anticipation commonly seen = increased number of repeats is inversely proportional to age of onset
      - mortality is usually due to falls or pulmonary infection
      - treatments: supportive, tetrabenazine, antidepressants, antipsychotics, high calorie diet
    - - caused by exposure to neuroleptics including antipsychotics and antiemetics
      - higher incidence in those being treated for Schizophrenia
      - can attempt treatment with VMAT2 inhibitors like deutetrabenazine, valbenazine, and acutely with Benadryl
    - - Tourette's = prototypical disorder
      - onset 5-10 years old
      - can resolve or be controlled by late teens/early 20s
      - treatment: VMAT2 inhibitors, antidopaminergics, stimulants for concurrent ADHD, antidepressants for anxiety/depression, CBT
    - - progressive, benign condition with hereditary/genetic implications with onset in early age (adolescence to late 20s)
      - typically bilateral
      - usually involves distal extremity flexor-extensor, high frequency/low amplitude movements of the hands
      - may be exacerbated by stress, anxiety, poor sleep, caffeine consumption
      - treatment: first line = primidone and propranolol; second line = Botox injections, DBS
    - - abnormal sustained contractions that are involuntary and often painful
      - can be primary (genetic) or secondary (acquired)
      - there are juvenile, adolescent and adult forms that are either static or progressive
      - characterization:
        
        anatomical location: focal, segmental, multifocal, generalized
        
        temporal pattern: persistent, action-specific, diurnal, paroxysmal
      - treatment: Gest antagonist, sensory trick, botulinum toxin injections, neuromodulation with DBS
- - - - focal-onset (originates in one hemisphere)
        
        aware vs impaired awareness
        
        motor vs non-motor onset
        
        focal to bilateral tonic-clonic
        
        narrow spectrum agents: phenytoin, fosphenytoin, carbamazepine, oxcarbazepine, ethosuximide, phenobarbital, vigabatrin, tiagabine, gabapentin, pregabalin, rufinamide
      - generalized-onset (both hemispheres)
        
        motor:
        
        tonic - muscle rigidity typically lasting <1 min
        
        atonic - sudden loss of muscle tone
        
        clonic - repetitive muscle jerking
        
        tonic-clonic - muscle rigidity and repetitive muscle jerking
        
        myoclonic - single rapid muscle jerks typically involving both arms
        
        non-motor:
        
        absence - staring spell +/- automatisms lasting <30 sec; abrupt onset & termination with amnesia, no post-ictal confusion; often triggered by hyperventilation; tx = ethosuximide
        
        broad spectrum agents: valproic acid, lamotrigine, topiramate, zonisamide, levetiracetam, benzodiazepines, clobazam, perampanel, lacosamide
    - - simple:
        
        age: 6mo - 5yr
        
        generalized onset
        
        <15 min
        
        one episode within a 24hr period
        
        FHx of febrile seizures
        
        normal neurodevelopment
        
        normal neurological examination
      - complex:
        
        age: <6mo or >5yr
        
        focal onset
        
        >15 min
        
        recurrence within a 24hr period
        
        often no FHx of febrile seizures
        
        may have developmental delay
        
        focal features or post-ictal deficit
  - - - continuous seizure activity or multiple seizures without return to baseline over a period >5 min
      - a neurological emergency
      - common etiologies: acute insult, low AED levels (missed medications), initial presentation of chronic epilepsy
      - treatment: ABCs, correct hypoglycemia if present, emergent parenteral anti-seizure medications (1st line = IV lorazepam; 2nd line = IV phophenytoin)
    - - oral/manual automatisms, contralateral dystonic limb posturing, spitting or vomiting, secondary generalization
    - - fencing posture, figure 4 sign, bicycling, windmilling
    - - no evident trigger
      - convulsions coincide with loss of consciousness
      - usually lasts 1-2 minutes
      - rhythmic bilateral synchronous movements
      - post-ictal obtundation >10min
      - can occur during sleep
      - eyes open 97%
      - no response to noxious stimuli
      - tongue biting may be severe
    - - sudden, unexpected death of someone with epilepsy who was otherwise healthy
      - no other causes of death are found on autopsy
      - each year, more than 1 in 1000 people with epilepsy die from SUDEP
      - RF: frequent generalized tonic-clonic seizures, subtherapeutic AED levels, AED polytherapy, early age of epilepsy onset/longer duration of epilepsy, young age, male sex, developmental delay