• Evaluate blood vessels • Aneurysm • AV malformation
plain film indications in nuero
• Evaluate for stenotic arteries in patients with TIA stroke
• Nerve Conduction Studies (NCS) –
integrity of peripheral nerves: axons, myelin
• Electromyography (EMG)
– electrical activity of muscle fibers
− Seizure, seizure disorder − Altered level of consciousness, coma − Encephalopathy
bacterial meningitis: etiology and pathophsyiology, RFs, clinical presetnation, lab findings, plan, sequelae of untx'd
Risk Factors • Exposure to meningitis • Travel to endemic areas- meningitis belt in Sub-Saharan Africa, important for travel exams • Respiratory tract infection • Injection drug use • Penetrating head trauma • Neurosurgery • Devices - shunt, cochlear implants Pathophysiology − Infections break down the blood-brain barrier and enter brain − Inflammation and irritation of meninges − Meningeal signs − Neurological complications − Cerebral edema Meningeal signs • Nuchal rigidity – stiff neck − Indicated by decreased neck flexion– inability to touch chin to chest or neck feels stiff when felt • Kernig’s sign- flex hip to 90° and patient doesn’t allow knee extension • Brudzinski’s sign- flex head and hip comes up sx Mild/moderate • Headache • Confusion • Irritability • Nausea • Vomiting sx severe Severe • Altered mental status • Cushing reflex- ↑BP and ↓ pulse • Papilledema- edematous look in the eye from ↑ cranial pressure • Cranial Nerve (CN) palsy • Herniation Systemic signs • Fever • Ill appearing • Pericarditis • Arthritis • Sepsis/septic shock • ARDS • N. meningitidis: Rash, Arthritis • Meningococcemia rash Physical Exam • Vital signs--temp • Meningeal signs − Nuchal rigidity – stiff neck − Often they can’t flex chin toward chest actively or passively. Document on exam or say “neck is supple” (normal) − Kernig’s (knee, can’t extend knee) − Brudzinski’s sign (when passively flex neck their hip will flex which is a reflex that takes pressure off spinal cord) • Neuro exam • Skin exam • Signs bacterial infection Labs • CBC, CMP, blood cultures (About 50% may be positive—not super helpful but if we can’t get a lumbar puncture its our best bet) • Lumbar puncture ASAP • Opening pressure elevated • Leukocytosis- can’t r/o with low WBC • Thrombocytopenia • PT/PTT- later stage • Electrolytes, BUN, creatinine, glucose tx: abx fatal if not tx'd
bacterial meningitis presentation in infants
Infants: • Fever • Hypothermia • Lethargy • Respiratory distress • Jaundice • Poor feeding • Vomiting • Diarrhea • Seizures • Restlessness • Irritability • Bulging fontanel Neonates • Temperature instability • Neuro signs: Irritability, lethargy, poor tone, tremors, twitching, seizures, bulging/full fontanel, nuchal rigidity • Other: Poor feeding/vomiting, respiratory distress, apnea, diarrhea
lumbar puncture side effects
• Post-LP headache • Infection • Bleeding • Cerebral herniation (since lowering pressure in spinal cord, risk that brain will herniate there) • Back pain • Minor neurological symptoms
ddx of meningitis
Differential Diagnosis • Fever − Pneumonia − Influenza − URI − Viral infection − Gastroenteritis • Headache − Subarachnoid Hemorrhage- sudden, worst headache • Nuchal Rigidity − Musculoskeletal causes − Injury − Arthritis − Sleeping position
aseptic meningitis patho, eti, clinical, dx, eval, tx
Pathophysiology • Mucosal surfaces of respiratory and GI tract • Viral replication in regional lymph nodes • Primary viremia – onset of illness and seeding of other organs • Second viremia - invasion CNS Symptoms • Viremia: − Signs of virus (viral exanthem) − Nonspecific viral symptoms − Fever, headache, malaise, myalgia, anorexia, nausea, vomiting • CNS invasion/meningeal inflammation: − Meningeal signs − Focal neurological deficits – less common Evaluation • Fever, headache, nausea, vomiting, photophobia, stiff neck Historical clues: • Travel history • Exposure to ticks and animals • TB risk factors • Sexual history (herpes, syphilis can cause it) • Exposure • Medications • Symptoms of specific viruses • Preceding illness Physical exam • Meningeal signs, neuro exam • Look for signs to suggest etiology • Rash, parotitis- mumps, genital lesions, thrush • Malignancy Diagnostic Tests • Labs – CBC, electrolytes, BUN, creatinine, glucose, blood cultures, PT/PTT Treatment • Still admit to hospital to follow them • Symptomatic treatment- can be outpatient − Analgesics, antipyretics, antiemetics − Fluids • Suspected viral − Antibiotics: elderly, immunocompromised, recently received abx (b/c at higher risk) − Observe: everyone else • Unclear viral or bacterial − Empiric antibiotics − Observe, repeat LP • Etiology confirmed- specific treatment as indicated
encephalitis dx, patho, tx, eti
• Inflammation of brain parenchyma • Primary viral infection − Viral invasion of CNS − Culture from brain tissue • Postinfectious − Virus cannot be detected or recovered − As initial infection is resolving or subclinical illness Etiology • Most viruses predominantly cause either meningitis or encephalitis: • Arthropod-borne viruses- West Nile Virus • Herpes viruses- see below • St. Louis encephalitis • La Crosse virus • Varicella-zoster virus • Epstein-Barr virus History • 7 attributes of symptom • Encephalitis symptoms • Regional exposure and outbreaks • Geographic location- CO tick virus, etc. • Exposure history (insects and animals) • Sexual history • Recent travel Symptoms • Abnormalities in brain function • AMS – confused, agitated, obtunded • Seizures • Motor or sensory deficits • Altered behavior and personality • Speech or movement disorders • Focal deficits of meningitis: − Hemiparesis − Flaccid paralysis − Paresthesias − CNS deficits • Lack meningeal signs (photophobia, nuchal rigidity) • Fewer nonspecific signs and symptoms − Many times have fever, headache, nausea/vomiting • May have signs outside CNS of specific virus Physical Exam • No pathognomonic signs • Altered mental status • Focal neurological signs Signs of underlying illness • Rash • Mumps – parotitis • West Nile virus − Flaccid paralysis − Maculopapular rash − Tremors eyelids, tongue, lips, extremities • Rabies − Hydrophobia, aerophobia, pharyngeal spasm, hyperactivity • Varicella-zoster virus – grouped vesicles in a dermatome Tests • Consider PCR (HSV-1, HSV-2, and enteroviruses), bacterial culture, fungal culture, mycobacterial tests and serology for arbovirus • CSF: confirm inflammatory disease of CNS • May look like viral meningitis • CT to rule out space-occupying lesions or brain abscess • MRI can detect demyelination • EEG often abnormal • Brain Biopsy – last resort, if still unclear etiology tx: sxatic
seizures: all possible causes
Etiology • Idiopathic • Degenerative: MS, presenile dementia- cause degradation of neurons or myelin sheaths • Infectious: meningitis, abscess, neurosyphilis • Metabolic: HYPOGLYCEMIA (easy to miss—if diabetic always check the blood sugar), hepatic failure, hyper-/hyponatremia- predisposing factor for electrolyte imbalance • Neoplastic: primary or metastatic tumors • Perinatal: infection, metabolic disorders (metabolites build up in brain)- newborns might be missing key enzymes • Toxic: theophylline, lidocaine (stabilizes neuronal membranes at therapeutic doses), TCAs, cocaine (and other street drugs) do a “tox screen” on anyone that prevents with a first time seizure • Head trauma: epidural/subdural hematomas, cerebral contusion • Vascular: stroke, Arterial Venous Malformation (AVM- clusters of dilated blood vessels susceptible to bleeds, AVMs in brain can cause seizures), subarachnoid hemorrhage (bleeds from aneurysm) • Eclampsia: pregnancy (preeclampsia↑BP, edema, and proteinuria- at risk for seizure → actual seizure=Eclampsia) (preeclampsia=toxemia of pregnancy) • Alcohol withdrawal- CNS depressant preventing seizure activity, withdrawal (usu 12-24 hr after last drink) removes that limitation
what are the phases of grand mal seizures?
tonic, clonic, post ictal
do petit mal seizures have post ictal phase?
no • Typically very brief (few seconds) • Abrupt LOC • Blank stare- eyelids may twitch • No response to voice • No falls, no involuntary movement, no incontinence- no tonic clonic behavior (Don’t lose muscle tone) • No post-ictal phase, attacks cease abruptly, patient unaware that
what are simple partial seizures?
• No alteration of consciousness (totally alert) • Manifestations may be: 1. Motor − Tonic or clonic movements, often unilateral, often limited to one extremity 2. Sensory − Paresthesias/numbness (can’t feel this half of my body…i.e.) − Flashing lights − Olfactory/gustatory (taste) hallucinations
what are myoclonic seizures?
• LOC associated with isolated jerking of one extremity • Unusual • Can have a post-istal phase after these as well • Still considered a generalized seizure because they have lost consciousness
what criteria fit a generalized seizures?
• Near-simultaneous activation of entire cerebral cortex • Causes abrupt LOC
what is a complex partial seizure?
• Involves AOC (alteration of consciousness) or mentation, lasting several minutes, no one set pattern, can present in a lot of ways • Usually bizarre symptoms with psychic features − Visceral symptoms (nausea, butterflies in stomach) − Hallucinations (visual, olfactory, auditory, olfactory) − Memory disturbances (déjà vu, jamais vu (should be familiar with something, like this classroom, but they aren’t) − Dream-like states − Automatisms: repetitive, purposeless movements (lip-smacking, playing with clothes) − Affective disorders (paranoia, depression, elation)
what's in the ddx for a seizure?
• Syncope: has premonitory feeling of “going to black out”, graying of vision, quick recovery of consciousness- may have sudden twitches from lack of oxygen to brain but lacks post-ictal phase • Narcolepsy: brief attacks of uncontrollable daytime sleepiness • Movement disorders (tics, jerks, tremors): consciousness preserved, movements involuntary but pt. can usually suppress it • Hyperventilation syndrome: gradual onset with SOB, anxiety, numbness of mouth/extremities (blood becomes alkaline), maybe LOC • Psychogenic seizures/Pseudo seizures
when would CT, MRI, EEG be used in people with seizures?
CT if first time to look for structural lesions but not established seizures pts, MRI for first time seizures to look for more subtle changes, EEG in everyone with first time seizure
what should all patients be warned about after having a seizure?
• No driving (until better handle on what’s going on—established criteria in consult with neurologist) • No operating dangerous machinery • No heights • No unsupervised swimming
status epileptics definition and causes, action steps (tx in pharm)
Continuous seizure activity lasting >30 min. or Two or more seizures without return of consciousness in between Causes of Status Epilepticus • CNS infection • Trauma • Anoxia • Noncompliance or change in anticonvulsant meds • Stroke • Metabolic derangements- glucose is most important, hypo/hypernatremia tx • ABC’s − O2 by facemask, consider intubation − Large-bore IV • Check stat glucose! − Administer D50 if hypoglycemic • Anticonvulsant therapy • Labs − Glucose, Electrolytes, BUN/Cr − Tox screen − Anticonvulsant levels − Serum CK for rhabdomyolysis • CT head after seizures controlled • IV antibiotics/LP if meningitis suspected
what is delirium?
• Transient, global disorder of cognition; also called ‘acute confusional state’ • Syndrome with multiple causes that result in a similar constellation of symptoms • Clinical hallmarks are decreased attention span and a waxing and waning type of confusion • Often unrecognized or misdiagnosed • Medical emergency associated with increased morbidity and mortality rates
these sx represent what disorder? • Transient, usually reversible, global disorder of cognition and consciousness • Develops over a relatively short period (hours to days)- dementia takes longer to develop • Fluctuates over the course of a day • most sx late in the day with a change in light “sundowning” • Cognitive impairment generally represents a significant change from baseline
possible causes in development of delirium
Common causes: • Toxins • Metabolic conditions • Infections • Endocrinologic conditions • Cerebrovascular disorders • Autoimmune disorders • Seizure-related disorders • Neoplastic disorders • Hospitalization • Terminal end-of-life delirium or D: Dementia E: Electrolyte disorders L: Lung, liver, heart (MI, HF), kidney, brain I: Infection R: Rx drugs I: Injury, pain, stress U: Unfamiliar environment M: Metabolic
what is the most common reversible cause of delirium?
• Medications are the most common reversible cause of delirium (22-39%)
what are risk factors for delirium?
Cognitive impairment (dementia, mental retardation) Sleep deprivation Immobilization Psychoactive medications Vision impairment Hearing impairment Dehydration
what are the types of deliirum/
• Hyperactive: Restlessness, agitation, fearfulness (can be subtle); associated with drug intake, alcohol withdrawal, amphetamines, PCP, LSD • Hypoactive: Lethargy, stupor associated with hypercapnia, hepatic encephalopathy (most common in patients > 65, easily missed or misdiagnosed as depression) scary b/c they can become dehydrated, immobilized • Mixed: Fluctuation between hyperactive and hypoactive; usually nocturnal agitation and daytime sedation
how would you manage delirium?
r/o preexisting causes, do cognitive testing, H&P, review med lest, eval labs (i.e. syphilis), search for occult infection, can do other tests (like tox, ABG, lumbar puncture for meningitis). create supportive and familiar environment (− Well lit, large clock, familiar items, uninterrupted sleep, family nearby, frequent staff checks)
what is dementia?
An acquired, sustained impairment in intellectual function with compromise in at least three of the following spheres of mental activity 1. Memory 2. Language 3. Visulospatial skills 4. Personality 5. Other instrumental cognitive abilities (abstraction, calculation, judgment) DSM-5 Diagnostic Criteria Evidence of significant cognitive decline from a previous level of performance in one or more cognitive domains: Learning and memory Language Executive function Complex attention Perceptual-motor Social cognition
potential causes of dementia
Degenerative AD, Huntington’s, Parkinson’s Vascular Cerebrovascular dz, vasculitis* Metabolic Uremia*, liver failure* Toxic EtOH*, medications*, heavy metals* Vitamin deficiency B12*, thiamine* Structural disease or trauma Normal-pressure hydrocephalus*, neoplasms*, dementia pugilistica (multiple concussions—repetitive traumatic encephalopathies) Intracranial space-occupying lesions Subdural hematoma, tumor* Anoxic Cardiac arrest, resp. failure*, CO poisoning* Infections CJD, HIV, neurosyphilis*, postencephalitis Endocrine Hypothyroidism*, ↓ Ca++* Psychiatric Depression*, schizophrenia* *Indicates reversible cause
what are the reversible causes of dementia?
uremia, liver failure, ethos, medications, heavy metals, b12, thiamine, hydrocephalus, neoplasms, respiratory failure, CO poisoning, neurosphyilis, tour, hypothyroidism, calcium, depression, schizophrenia
what parts of the brain are affected in cortical dementia (like AD)
Temporal cortex (medial) Parietal cortex Frontal lobe cortex
what parts of the brain are affected in subcortical dementia (like parkinson)
Thalamus Striatum Midbrain Striatofrontal projections
what is vascular dementia?
• Second most common cause of dementia • May result from multiple infarcts (multi-infarct dementia), strategically placed single infarcts, small vessel disease with subcortical ischemia, hypoperfusion, amyloid angiopathy, brain hemorrhage, and some inherited disorders of blood vessels • Tends to have an earlier age of onset, affects more men than women, and a shorter duration of survival after onset than AD • Patients often have risk factors such as HTN, DM, hyperlipidemia, and cigarette smoking • Cognitive dysfunction can develop abruptly, and patients may experience stepwise deterioration or have a history of TIAs • May be focal signs on neuro exam • Deficits include early incontinence, gait disturbances and flattening of affect
what is levy body dementia/
• Eosinophilic inclusions (Lewy bodies) in subcortical neurons of patients with Parkinson’s disease • Accounts for 15-25% of all degenerative dementias • Shares clinical and pathologic features with AD- may be considered a variant of AD • Regarded by some as an AD variant • Clinical features: Dementia and at least 2 of the following: Fluctuations in cognition, visual hallucinations, and parkinsonian motor signs • Patients have slowed cognition and impaired attention, otherwise similar to AD • Consider it with bizarre, erratic behavior and no response to medications
what is frontotermporal dementia/
• In 1906, Arnold Pick identified a progressive behavioral disorder associated with bilateral frontal lobe atrophy with intraneuronal inclusions (pick bodies) • Bilateral frontal lobe atrophy with intraneuronal inclusions (Pick bodies) • Frontotemporal dementia describes patients who have Pick’s disease with Pick bodies, or frontotemporal atrophy without Pick bodies, and frontotemporal atrophy with motor neuron disease • Frontal lobe- planning, inhibition, executive actions • Remain fluent with phonation but have progressive difficulty with naming and word comprehension. Preserve memory, spatial skills, and praxis but executive function, emotional regulation and conduct impaired.
creutzfeldt jakob dz
• Prion disease in the family of transmissible spongiform encephalopathies • thru contaminated meat, not person to person • Affects about 1/1,000,000 per year • Typical onset of symptoms occurs about age 60 and 90% of patients die within 1 year • Early stages are characterized by failing memory, behavioral changes, lack of coordination and visual disturbances, myoclonus (muscle twitching) • With disease progression, mental deterioration becomes pronounced and involuntary movements, blindness, weakness of extremities, and coma may occur
patho pays of AD
abnormally processed amyloid precursor protein (beta-amyloid) (EXTRACELLULAR) accumulations of the cytoskeletal protein tau • Healthy neurons have microtubules that act like tracks, guiding nutrients & molecules to end of axon & back • Tau makes those tubules stable, but in AD tau is chemically changed (hyperphosphorylated) • Hyperphosphorylated tau pairs with other threads of tau & becomes tangled inside nerve cell bodies→ neurofibrillary tangles→ nerve cell death (INTRACELLULAR)
genetic influences in AD
• Early Onset Familial AD − About 5% of all AD cases − Majority of patients with EOFAD have autosomal dominant AD − Three genes identified, all result in ↑ production of β amyloid: PS1(Presenilin 1), PS2, APP (amyloid precursor protein) • Late Onset Familial AD − 15-25% of all AD − Majority of LOFAD is of complex inheritance via “susceptibility gene” APOE (apolipoprotein E) • Sporadic APOE • Environmental factors, e.g. head trauma, affect both (? familial late onset > familial early onset)
how do you dx alzheimers?
history: onset, time course, meds, any other illnesses. tests: baseline cognitive testing (mini mental status exam, neuropsych testing, depression)
what tests would be recommended to r/o other causes of alzheimers?
Recommended Rules Out Recommended Rules Out • CBC • Infection • LFTs • Liver failure, hepatic encephalopathy • Electrolytes r/o Ca¬2+ • Depression screening r/o Depression • Glucose r/o Hyperglycemia • Head CT/MRI r/o Subdural hematoma, trauma • Cr/BUN r/o Renal function If indicated: • Serum B12 levels r/o Vitamin deficiency VDRL/RPR- syphilis test r/o Neurosyphilis • TSH r/o Hypothyroidism • Lumbar puncture r/o Normal pressures
what should be included in family education for pt with dementia?
• Education of patient and family/caregivers is very important (Recommendation from the California Workgroup on Guidelines for Alzheimer's Disease Management, 2008) • Discuss diagnosis, progression, treatment choices and goals of AD care with patient and family in a manner consistent with their values, preferences and the patient’s abilities • Refer to support organizations for educational materials on community resources, support groups, legal and financial issues, respite care, future care needs and options − Alzheimer’s Association www.alz.org − Family Caregiver Alliance www.caregiver.org − Clinic social services department • Discuss the patient’s need to make care choices at all stages of the disease through advance directives and identification of surrogates for medical and legal decision-making • Discuss the intensity of care and end of life care decisions with the patient and family • Be aware of caregiver stress
what are ways to differnetiate delirium from dementia?
delirium is acute and fluctuating, and only lasts days to weeks. patients with delirium have altered consciousness whereas those with dementia have clear. pts with delirium will have altered attention but those with dementia will have pretty good attention.dementia is rarely reversible whereas delirium is, and delirium is usu caused by non brain causes whereas dementia is caused by brain dz
what's your assessment? Ms. Smith is an 83-year-old woman who has Alzheimer's dementia and cannot care for herself. She is ambulatory in a special care unit, but requires assistance with activities of daily living. Her memory deficit has been very gradually progressive; she continues to generally recognize family members and enjoys meals and activities. Her past medical history includes s/p TAH-BSO, cholecystectomy, a basal cell carcinoma removed from the left arm, and presbycusis. She uses glasses and a hearing aid. She is on no regularly scheduled medications in the nursing home. The nursing staff from the nursing home report that over the past few days she has become more confused and she has not been taking part in activities. She has had increased episodes of incontinence over the past couple of days and is eating less than usual. Her family is concerned because she did not recognize them this morning when they came to visit
Assessment: Delirium from UTI- treat UTI, delirium will subside
what's your assessment and plan? Mr. Jones is a 79-year-old man who was admitted to the hospital for an elective transurethral resection of the prostate (TURP) for moderate benign prostatic hypertrophy symptoms not responsive to medication therapy. Other stable medical problems include coronary artery disease, hypertension, and bilateral cataracts. Medications before admission were ASA 81 mg daily, diltiazem CD 180 mg daily, HCTZ 25 mg daily, and finasteride 5 mg daily. He is a retired businessman who lives alone. He quit smoking 10 years ago when he had an MI; he drinks wine with dinner. He is independent, still drives, and spends time with family and friends regularly. After an uneventful surgical procedure, he is put on standard post-up orders. On the evening of the second hospital day Mr. Jones begins to exhibit some fluctuation in level of alertness and has some confused content in his communications with his nurses and family members.
Delirium- unfamiliar environment, opioids for post-op pain management, potential catheter- consider changing analgesic to non-opioid medication, bring in familiarity, remove catheter¬
parkinsons: eti, epi, pathpphys, features, dx, tx
epi: 1% affected over 60 pathophys: • Lesion occurs at substantia nigra • Hallmark: Lewy body- pink mark/collection of proteins (synuclein protein aggregation) on the substantia nigra cell is the hallmark of PD striatal dopamine depletion feautres: • Resting tremor- distinguishes PD from other diseases (pill rolling look) often most apparent when sitting still, can be somewhat suppressed if moving or muscle contracted (20-25%) • Bradykinesia • Rigidity (might have stiffness or cramping on one side +/- tremor) • Posture/balance changes (can be lopsided or worse on one side) arm doesn’t move when walk, stooped over • Insidious onset, often unilateral • Patient may complain of voice change (gets quieter), small handwriting, change in gait dx on h&P and rulin gout other cases of parkionsonsims non motor changes: • Sleep: REM behavior disorder (no paralysis during dreams but may yell, kick—bothers bed partner), restless legs, depression, wearing off of PD meds, nocturia, pain • Autonomic nervous system: constipation, bladder urgency, drooling, orthostatic hypotension, abnormal sweating • Skin: 2 to 6-fold increased melanoma risk in people with PD and 1.5-fold higher incidence of PD in people with melanoma tx: none, static with dopamine and exercise
risk factors for parkinson
Environmental • Good: coffee, cigarettes, estrogen, exercise • Bad: rotenone, herbicides, welding, head injury Genetic • LRRK2 variants account for 8% of “familial” PD and some “sporadic” PD • At least 10 different genes implicated in PD • Parkin gene important in young-onset PD (
how do you tell the difference between parkinson and these other movement disorders?• Disorders that begin with Parkinson’s-like symptoms but progress in other ways • Progressive supranuclear palsy- • Corticobasal degeneration- • Lewy body disease- • Shy-Drager syndrome- • Multiple systems atrophy-
• Disorders that begin with Parkinson’s-like symptoms but progress in other ways • Progressive supranuclear palsy-no tremor; unable to look up/down, rigidity of trunk, falling • Corticobasal degeneration-unilateral tremor, apraxia, “alien limb” • Lewy body disease-PD with simultaneous dementia, hallucinations • Shy-Drager syndrome-PD with severe autonomic dysfunction • Multiple systems atrophy-ataxia, neuropathy, other “systems”
how should parkinson dz be managed/
early dz; wellness, education mid stage; lifestyle changes, ceasing some important activities, non motor sx, meds wear off end stage: safety, quality of life, needs assistance in daily life
what are the most common COD in parkinson patients?
• The most common causes of death: pulmonary infection/aspiration, urinary tract infection, pulmonary embolism and complications of falls and fractures
what is restless legs syndrome? mean age of onset, patho pays
Characterized by... 1. Desire to move in association with paresthesias/dysesthesias of the limbs 2. Motor restlessness Often confused with periodic limb movements of sleep=involuntary movements during sleep that bed partner will complain about. But restless legs is a creepy crawly feeling that makes you want to move your legs around. mean age of onset=27years majority are familial, can get secondary from other causes: • Renal failure • Iron deficiency • Neuropathy • Radiculopathy • Diabetes • Pregnancy • RA • Edema (stretching soft tissues) pahto phys • CNS abnormality (cerebral generators) • Dopaminergic dysfunction (of enzyme that makes it that uses iron as a cofactor…not degenerative of neurons that use it) • Disinhibition of the flexor reflex during sleep • Possible involvement of the endogenous opiate system
essentia tremor: definition, classifications
Bilateral (PD usu one side), postural or kinetic tremor involving the hands and forearms • Tremor is persistent and visible or • Additional or isolated tremor of the head in the absence of abnormal posturing classifications: • Rest tremor- common in PD • Action tremor − Postural tremor − Kinetic tremor − Task- or position-specific tremor
what do each of these signs with tremor mean? 1. Unilateral tremor, focal tremor, leg tremor, gait disturbance, rigidity, bradykinesia, rest tremor 2. Sudden or rapid onset 3. Current drug treatment that may cause or exacerbate tremor 4. Isolated head tremor with abnormal posture
1. Unilateral tremor, focal tremor, leg tremor, gait disturbance, rigidity, bradykinesia, rest tremor--parkinsons 2. Sudden or rapid onset 3. Current drug treatment that may cause or exacerbate tremor 4. Isolated head tremor with abnormal posture (head tilt or turning is probably dystonia from torticollis)
what are some ways to "tx" or overcome essential tremor?
• No treatment—how bad is it? She discourages it in the older pop. • Psychological measures/lifestyle changes-wrist weights, biofeedback, bigger pens (hand in more relaxed position) Pharmacologic approaches: • Beta-blockers • Primidone (barbiturate) • Benzodiazepines (can be used prn) Surgery-thalamic stimulation
neurologic movement disorder characterized by sustained muscle contractions that frequently cause twisting or repetitive movements and abnormal, sometimes painful, postures or positions.”
what is the difference between primary and secondary dystonia?
primary : its the only sign; secondary can be d/t parkinsonism, post traumatic, drugs
what are some examples of focal dystonia?
• Blepharospasm- eyelids shut • Oromandibular dystonia • Meige syndrome • Cervical dystonia (spasmodic torticollis) • Laryngeal dystonia (spasmodic dysphonia; abductor or adductor types)- most common form in the US • Limb dystonia (task-specific dystonia - writer’s or musician’s cramp)
what important things should be considered in the hx of someone suspected of having dystonia?
• Secondary dystonia may present months or years after the initial cerebral insult • Exposure to drugs: anti-dopaminergics (e.g., neuroleptics, anti-emetics, anti-vertiginous agents) • Toxins: manganese, methanol, cyanide, etc. • Trauma: birth asphyxia, peripheral trauma, etc.
what is spasticity?
“Spasticity is a motor disorder characterized by a velocity-dependent increase in tonic stretch reflexes (muscle tone) with exaggerated tendon jerks, resulting from hyperexcitability of the stretch reflex, as one component of the upper motor neuron syndrome.” It’s like a clasped knife if you try to move their limbs and then suddenly it gives. Whereas Parkinsons stiffness is called “lead pipe” and its stiff all the way through.
what is ataxia and what is a good way to test for it?
• Dysmetria of eye movements, nystagmus (eyes wiggle when at extreme of lateral or medial) (sichatic eye movements—have them jump eyes from one of your fingers to the other their eye will overshoot and have to wiggle back) • Dysarthria (dysregulated speech: slurred or explosive) • Limb dysmetria (clumsy hitting a target), incoordination (can’t do movements smoothly) • Gait ataxia • Finger to nose test (quickly but accurately touch tip of finger), rub heel on opposite shin • Indicates cerebellar problem, esp if smack face when trying to hit nose
what is hunting tons disease?
• Movement disorder − Chorea (same as dyskinesia), other involuntary movements − Later dystonia − Voluntary motor dyscontrol − Premotor planning affected • Cognitive disorder (dementia) • Emotional disorder − Includes depression, anxiety, obsession, paranoia
what is the genetic basis of huntingon's dz?
automsomal dominant disorder with CAG repeat in huntington's gene
huntington's dz: diagnostic eval, pathophys
dx: MRI Scans in HD • Shrinkage of the caudate nucleus is indicative of HD (near the central dark portion of the ventricles) genetic test path physDegenerating cells develop intranuclear inclusions of abnormal huntingtin protein
how do you manage huntingnont's dz?
meds for sx, PT, OT, nutrition, social services, genetic counseling, care of families, psych/neuropsych assessment and counseling
when infarcted, which area of brain will cause these sx? • This artery supplies area of brain for speaking • Most common • Large infarction with contralateral weakness/hemiplegia (face and arms > legs) • Conjugate eye deviation toward the side of the infarct/lesion, hemianesthesia. Even if you say look over here, they won’t do it. • LEFT side: Brocas (expressive) aphasia –difficulty speaking, understanding OK and Wernickes (receptive) aphasia—fluent speech but not making sense--commonly seen together • Associated global aphasia if the dominant hemisphere and hemineglect with nondominant hemispheral lesions. • RIGHT side: Neglect. They might completely ignore one hand when both presented together, even if they can ID both on their own. Might not even
middle cerebral artery
what's the difference between a stroke and a TIA?
RFS for stroke: modifiable and non modifiable
modifiable: HTN, etoh, afib, HLD, obesity, sedentary life style, smoking, DM, estrogen use, cardiac dz (like prostethic valves, cardiomyopathy, Pfo) nonmodifiable: age, race, family history, genetic hyper coagulable states
differing pathophys of ischemic vs. hemorrhagic vs cerebral aneursm
ischemic strokes can be cause by a thrombus/embolus or dissection within that vessel; hemorrhagic are caused by bleeding out that causes loss of blood distally, aneurysm do not cause blood loss unless grow to big and bust
clinical presentation of stroke vs. hemorrhagic stroke
stroke is usually painless with focal near deficits while hemorrhagic is usually painful
what kind of stroke is caused by atherosclerosis?
large artery thromboembolic
what type of stroke is caused by emboli from hear?
what type of stroke is caused by untreated HTN?
small vessel lacunar
what type of stroke presents with head/neck pain?
dissection of carotid or vertebral arteries
ddx of stroke
• Hypertensive Encephalopathy • Epidural/subdural Hematoma (hemorrhagic stroke) • Demyelinating Disease (MS) • Drug Toxicity (lithium, dilantin, Etoh) • The bends • Conversion disorder • Tumor • Migraine • Seizure (Todds paralysis) • Hypoglycemia/Hyperglycemia Bell’s Palsy
area of brain: contralateral weakness and sensory loss in R leg, +/- aphasia, impaired memory or emotional disturbances
Left anterior cerebral
area of brain associate with amaourosis fugax
intenral carotid/retinal arteyr
area of brain associated with stroke causing left half of page to disappear (field is cut)
area of brain affected by stroke causing dysarthria (feel like drunk when talking), dysphagia, vertigo, gaze palsy
area of brain affected by stroke with sx of Ipsilateral Ataxia • Vertigo • Nausea and Vomiting • Nystagmus
when is MRI indicated over CT for stroke?
CT initially to r/o bleed before giving tpa. mRI good later on, esp if been a while since sx started
initial management of storke
CT to see if d/t hemorrhage, mRI for location, size, iv TPA, MRA or CTA of head and neck, EKG, echo, blood glucose, BP and lipids, hyper coagulable work up in young
what are some common migraine precipitants?
Migraine Precipitants • Menstruation (pre or mid cycle) • Too little/too much sleep • Fasting • Physical activity • Stress • Tyramine-containing foods- Red wines, Hard cheeses, Herring • Phenylethlamine- chocolate • Nitrates- processed meats • Caffeine withdrawal or excess- vasoconstrictor • Medications- OCP’s- can cause or prevent migraines, antiHTNs- affect vasomotor tone
common migraine characteristic
• Represents vast majority of migraines • Usually lasts 4-72 hrs • Characteristics: − Unilateral, Intensity: moderate to severe − Pulsating- intense vasoconstriction, followed by vasodilation − Aggravated by physical activity − Nausea/vomiting- very common − Photophobia/phonophobia • Patient should have at least 5 attacks before dx. madecommon migraine
what's different in the "classic migraine" from common migraine? describe it.
Aura. Aura comes on gradually, usually lasts
where can headaches and migraines occur in the head?
extracranially (muscle, BVs, periosteum), intracranially (BVs, venous sinuses, dura, falx cerebri) but NOT BRAIN PARENCHYMa
prophylactic meds for migraine
• Beta-blockers- most common prophylactic treatment, decrease blood flow to the brain and vasodilation − Propranolol • Calcium-channel blockers- smooth muscle relaxation → vasodilation − Verapamil • SSRI’s- decrease frequency of migraines − Paroxetine (Paxil), Fluoxetine (Prozac) • Tricyclic antidepressants − Amitriptyline, Nortryptaline • Anti-seizure meds- stabilize neuronal membranes − Valproic acid (Depakote), − Gabapentin (Neurontin)
abortive tx of migraines
OTC analgesics, ergots, anti-emetics, serontonin agonists, IV/IM NSaids, narcotics, steroids
when do most migraines usu start in life?
adolescence or young adulthood
what kind of HA? usu in males, usu stabbing (not throbbing), unilateral, trigeminal nerve involved (behind eye), +/- lacrimation, conjunctival injection, nasal congestion/rhinorrhea, ptosis, /miosis; usually a few in a row every few years
tx of cluster headaches
o2, same meds as migraine except no beta blockers
what kind of hA?• Duration: 30 min.-7 days • Contraction of muscles for a long period of time − Pressing/tightness/band-like (usually non-pulsating) − Mild-moderate intensity − Unaffected by physical activity − Possibly associated with photo-/phonophobia − Usually without nausea/vomiting
ddx of hA
Subarachnoid hemorrhage Meningitis Hypertensive headache Subdural hematoma Epidural hematoma Brain tumors/cerebral mets Migraine Cluster HA Tension HA Sinusitis Acute glaucoma Temporal arteritis Trigeminal neuralgia TMJ
what causes tension headaches?
contraction of muscles/band like
signs of a subarachnoid hemorrhage and management
sudden onset, "worst HA of my life", lOC, focal neuro signs, may have seizure, nuchal rigidity, need urgent ct (look for bright white blood) and need a cerebral angiography to visualize. tx with surgery or endovascular surgery (coil)
how do brain tumors present?
often progressively worsening over days to weeks/months. starts mild and stays there, doesn't go away and may be progressively getting worse; worse in the morning +/- am vomiting. may also have motor/sensory deficits, ataxia, vision loss, seizures, altered mental status
gold std for dxing brain tumors
most common primary brain tumor of brain
tx of astrocytoma
surgery + radiation +/- chemo
Progressively worsening over days to weeks (not acute and sudden like subarachnoid hemorrhage)
Often is worst in the morning, with AM vomiting- interstitial fluid when lying flat
Weakness, paralysis, sensory deficits, cranial nerve palsies
Altered mental status
Seizures- CT after first sz
Second most common type of brain tumor (2/100,000)
Arise from the meninges
Commonly on surface of brain, in concavity of skull
May be single or multiple
tx of meningioma
Observation- if tumor is small and asymptomatic
Need regular follow-up imaging
Surgical- Best results if tumor is superficial and easily accessible
Radiation- If surgical resection is incomplete or for recurrence
chemo not effective
Unilateral hearing loss
The most common presenting symptom
Can be sudden, persistent or fluctuating
Facial numbness or weakness- compression of brainstem and facial nerve
acoustic neuroma--notice how the tumor is in the cerebello pontine angle
tx of acoustic neuroma
surgery (by expert), radiation (palliative to reduce tumor), can just observe if older and symptoms not too bad (won't die form these)
T or F: cerebral metastases are more common than primary brain tumors
T; 1 in 5 cancer patients will have cancer go to brain. usually d/t lung or breast cancer
multiple lesions found in brain is usu d/t what? tx?
mets; need sysemic workup: CXR, chest CT, abdomen, pelvis
tx of cerebral mets
whole brain radiation therapy to get mets you can't see, can do stereotactic radiosurgery +/- chemo; surgery if
Solitary lesion > 3 cm
Lesions in “noneloquent” portion of brain
Limited systemic disease
One symptomatic lesion with multiple asymptomatic lesions
Symptomatic lesion resected, remaining lesions radiated
what do these red flag signs make you think of?
First severe HA or worst HA of pt.’s life, especially if acute onset
HA that gets progressively worse over days to weeks
Severe HA with fever
Decreased LOC or focal neuro signs
First severe HA or worst HA of pt.’s life, especially if acute onset (subarachnoid hemorrhage)
HA that gets progressively worse over days to weeks (tumor)
Severe HA with fever (meningitis)
Nuchal rigidity (meningitis or subarachnoid hemorrhage)
Decreased LOC or focal neuro signs (bad—work up; subarachnoid hemorrhage or tumor)
RFs: geography : 37th parallel, caucasians of scandinavian descent, age (younger onset in women), smoking, low vitamin D, some genetic involvement
eti: autoimmune, t cells attack myelin, Cd4 cells activiated and leads to inflammation and damage, possibly microbial? no one bug ID'd yet
pathophys: t cells attack myelin, inflammation by cd4, macrophages come in and "clean up"
The end result is a shrunken area of demyelination called a plaque, or sclerotic area
The axon cylinders and cell bodies are not destroyed, although the scar is capable of damaging the under lying axon fiber so that nerve fiber conduction is disrupted
Psychological changes(anxiety, depression)
signs of mS:
optic: blurred vision, color disturbances
motor:hyperreflexia, spasticity, paraparesis, dysarthria, babinksi
sensory: lhermittes sign, + rombergs, decrease in sensory and proprioception (dorsal column)
cerebellar: ataxia, finger to nose test bad, heel to shin, loss of speech
other: urinary incontinence, sexual dysfunction, cognitive and emotional abnormalities, fatigue, difficulty swallowing, dystonnia, +/- trigeminal neuralgia
these signs on mRI are indicative of which diease?
Plaques anywhere within the white matter of the CNS
↑ in immunoglobulin concentrations in the CSF studies in more than 90% of patients with MS.
IgG index (a comparison between IgG levels in the CSF and in the serum) is elevated in many MS patients.
Oligoclonal Immunoglobulin Bands can be identified in the CSF of MS patients via electrophoresis. (if you see this, ITS MS!)
The overall protein level is also slightly elevated - up to 0.1 g/
· On T-2 weighted images, patchy areas of abnormal white matter (ovoid white lesions) are found most commonly in cerebral hemispheres in periventricular areas; can be present in the cerebellum and brain stem, cervical and/or thoracic spinal cord
· Gadolinium enhancement on the MRI scan is considered a sign of an active lesion
gold std test for MS
· Total volume of T2-weighted lesions (called T2 burden of disease) shows a significant (although weak) correlation with clinical disability in which disease?
differential dx of ms
Any other condition that may potentially affect the nervous system, e.g.
CNS vasculitis, especially lupus
Nutritional disorders, e.g. Vitamin B12 deficiency
Often will do a rheumatoid type workup: ANA, sjogren’s, vitamin D; anything that can cause vague sx of fatigue
Accounts for 85% of MS cases at onset
Characterized by discrete attacks that generally evolve over days to weeks (rarely over hours)
Often, but not always, there is complete recovery over ensuing weeks to months
When ambulation is severely impaired during an attack, ~ 50% will fail to improve
Between attacks, patients are neurologically stable
Disease progression associated with more frequent attacks, tx aimed to prevent those relapses/attacks
relapsing remitting MS
Always begins as RRMS
A steady deterioration in function unassociated with acute attacks (which may continue or cease during the progressive phase)
Approximately 50% of patients with RRMS will have developed SPMS after 15 years
Appears to represent a late-stage of the same illness as RRMS
secondary progression MS
Accounts for ~15% of MS cases
Patients do not experience attacks but only a steady functional decline from disease onset
Disease begins later in life (mean age 40 years) and disability develops faster
primary progressive ms
Overlaps PPMS and SPMS and accounts for 5% of patients
Patients experience a steady deterioration in their condition from disease onset—never get back to baseline like in RRMS
They experience occasional attacks superimposed upon progressive course
Early stages are indistinguishable from PPMS
progressive relapsing ms
patient education for ms patients
· Multiple issues necessitate a team approach to care
Patient Education- Educate the patient and their family about MS (www.nmss.org) get involved early
1. Life adjustments: Grief and loss, Depression common (suicide risk), Unknown future, walking devices, OT
2. Financial and Vocational Issues: Cost of therapy, Continued employment, Cognition
3. Sexuality, Family Issues & Pregnancy
Physical Therapy- mobility issues
Occupational Therapy- ADLs and job skills
Speech Therapy- swallowing problems
Vocational Rehabilitation- helps patients maintain their current job or find other employment opportunities despite disabilities
Goal: optimize function and QOL
differential diagnosis for neurological diseases
Cerebrovascular diseases - CVA, subdural or epidural hematoma
Demyelinating diseases - MS, Guillan-Barre
Amyotrophic Lateral Sclerosis
Neuromuscular Disorders - myasthenia gravis, botulism, organophosphate poisoning. Lambert-Eaton myasthenia syndrome
Focal neurological diseases - trauma, tumor, inflammation, radiculopathies (cervical, lumbar)
Neuropathies - peripheral, nerve plexus
Spinal cord disease - injury, spinal muscle atrophy, disc disease
Infectious - Influenza, EBV
Drug-induced - Alcohol, Corticosteroids, statins
Endocrine - Adrenal insufficiency, Glucocorticoid excess, Hyperparathyroidism, Hypo and hyperthyroidism, acromegaly, hypopituitarism, Vitamin D deficiency
Inflammatory - Polymyositis, dermatomyositis, vasculitis
Rheumatologic – arthritis and autoimmune (RA, SLE)
Genetic - Muscular dystrophy
Metabolic - Disorders of carbohydrate,lipid metabolism
Electrolyte disorders – hypocalcemia- ¯ threshold potential, hypercalcemia- threshold potential, hyper and hypo -kalemia and –magnesemia
Amyloidosis and sarcoidosis
Various uncommon genetic and metabolic diseases
meds that can cause motor weakness
infections that can cause motor weakness
motor weakness emergencies
Respiratory muscle weakness
Tachypnea- consider Mechanical ventilation
Pharyngeal muscle weakness
Dysphagia, dysarthria- Intubation
MG, dermatomyositis, polymyositis, West Nile Virus
Spinal cord compression
causes of generalized weakness
causes of asymmetric weakness
Multiple Sites- Multiple Sclerosis
Unilateral- Cerebrovascular or spinal cord disease
causes of symmetric with proximal distribution weakness
Unable to rise from a seated position without the use of the upper extremities
Unable to perform a deep knee bend
Difficulty combing hair
Duchenne Musclular Dystrophy
Guillan Barre Syndrome
weakness with distal distribution causes
Decreased grip strength
Weakness of wrist flexion or extension
Decreased plantar flexion strength, and foot drop
Difficulty walking on heels or toes
Peripheral neuropathy –
Accompanied by sensory deficits
DM, alcoholism, HIV
characteristicd of uppe rmotor neuron issues and causes of upper motor neuron issue
babinski, hyperreflexia, spasticity, clonus; stroke, tumor, demyelinating, infection, trauma
lower motor neuron lesion characteristics and causes
atrophy, flaccidity, fasiculations, fibrillations, hyporeflexia
Lead poisoning, poliomyelitis, West Nile Virus, ALS, spinal muscular atrophy, Charcot-Marie-Tooth disease, progressive muscular atrophy, neuropathy
lesion in muscle or myopathy: characteristics and causes
Findings: weakness, extramuscular symptoms
May have normal or atrophied (replaced with scar tissue w/ contractures) or pseudohypertrophied bulk, normal or decreased tone, proximal distribution, normal or decreased reflexes
weakness d/t neuromuscular jcn: characteristic and cause
Progressive muscle weakness
Myasthenia Gravis- Anti-ACh receptor antibodies
Organophosphate poisoning- inhibits Ach ( insecticides)
Lambert-Eaton syndrome- Interferes with presynaptic Ca2+ channel function
Normal bulk, bone, reflexes
what do each of these assoiated symtpoms mean when combined with weakness?
Stones, bones, abdominal moans
Legal problems, memory loss, unexplained trauma
Relapsing and remitting symptoms
Stones, bones, abdominal moans – hypercalcemia
Rash – SLE (malar), dermatomyositis- Heliotrope: dermatomyositis around eyelids
Truncal obesity – Cushing’s syndrome
Legal problems, memory loss, unexplained trauma – alcoholism
STD – HIV, syphilis
Relapsing and remitting symptoms – MS
focal sensory loss causes
UE – carpal tunnel
LE – back pain and radiculopathy
Peroneal neuropathy - crossing legs
Signs and symptoms in nerve distribution
Numbness, tingling, pain
multifocal sensory loss causes
Sensory ataxia, absent reflexes, dysesthesia
No motor involvement
Sjogrens, DM, Sarcoidosis, HIV
multifocal symmetric --proximal sensory loss causes
Proximal is usually predominantly motor
What is the pattern/distribution?
multifocal symmetric distal sensory loss causes
Length dependent neuropathy – affects longest axons first
DM, alcohol, HIV
What is the pattern/distribution?
when should you check visual acuity
Before any testing to the eye or adnexa is done.
This is the very first test!
these initial signs are supportive of what dx?
sensory loss, optic neuritis (vision changes, blurred or color changes), weakness, paresthesias (lhermitte's sign)
>2 lesions in space and time on T2 weighted MRI images
will show patchy, ovoid white lesions of abnormal white matter
or increase in immunoglobulin concentrations in CSF or oligoclonal immunoglobulin bands
ddx of ms
lyme, rheumatologic conditions work up (ANA, etc), stroke/tia, sarcoidosis, syphilis, hIV, nutritoinal disorders
what's the most common type of ms at onset? what are the other types?
relapsing remitting. other types are secondary progressive, primary progressive and progressive/relapsing
what test helps assesa and measure neuro impairmet in mS patients?
kurtzke expanded disability status score
term: disruption of normal vision development
inflammation of cornea
squamous epithelium membrane covering globe
ectoprion and entropion: eyelids turn outward or inward
what's a distinguishing feature of viral conjunctivitis?
usually watery, almost ALL are viral.
gradual onset of
Fixed deep injection of the blood vessels on the sclera
Hallmark is deep, throbbing, severe pain that may radiate to jaw or temple
Photophobia, Tearing, pain on palpation of globe, edema
Drainage cannot occur, pressure increases, PAINFUL
Only form of glaucoma with sx
They feel like they are going to vomit, head feels like its going to blow up, ER worthy
pathology of anterior chamber angle=acute angle closure glaucoma
different sizes of pupils
Dark unreflective layer, between the sclera and retina
Absorbs light and stops reflection.
Contains pigment and rich blood vessels
Pain, decreased VA, photophobia, pupil irregularities (miosis or constricted) what has to be on your ddx b/c its severe??
#1 cause of flashes and floaters; what else has to be on your ddx?
posterior vitreous detachment but need to refer in case of retinal detachment
: restoring pain-free function of the legs, back, neck, shoulder, and torso, restoring independence and safety in transfers and gait
: restoring function of the upper extremity, especially hand therapy, as well as ADL’s and cognitive training to assist with planning and performing ADL’s
is working on cognition, sensory processing, ADLs, a part of PT or OT?
what are some important things to condsider before discharging someone--aka red flags that they need more care or supervision?
if can't do ADLs safely, can't take meds, can't handle emergencies, etc.
what test scales cognition in someone recovering from a brain injury?
what is the best way to referr to pT/OT/
Do not specify # of visits- patient may plateau sooner but still want to come to PT, insurance will not cover sessions if no progress is being made
Orders are best scripted as “evaluate and treat”- allows more freedom for therapist to treat