neurology

GLUTAMATE EXCITES NEURONS, NMDA RECEPTOR USES GLUTAMATE NEUROPLASTICITY,

GABA IS AMNO ACID FORMED FROM GLUTAMATE W ADDITION OF VIT B6 AND ANOTHER THINGS -ONCE FORMED IT IS USED TO FORM SUCCINATE AND ENTERS POST SYNAPTIC TERMINALS OF NEURONS AND INHIBITS.IT IS AN INHIBITORY NEUROTRANSMITTER

WHEREAS GLUTAMATE HAS NMDA AS RECEPTOR INTO NEURON

GABA N/T HAS GABA RECEPTORS -GABAa and GABAb INTO NEURON

GABAa IS FAST SYNAPTIC INHIBITION

GABAb IS SLOWER SYNAPTIC INHIBITION

UPPER : START IN CORTEX GRAY MATTER 4 LOBES AND TRAVEL DOWN BRAIN AND TO SPINAL CORD

LOWER:START IN SPINAL CORD AND GO ON TO INNERVATE MUSCLES AND GLANDS THROUGHOUT THE BODY

UMNS USE GLUTAMATE

LMNS USE ACETYLCHOLINE

To perform a movement, a signal must begin in the primary motor cortex of the brain, which is in the precentral gyrus. In the primary motor cortex are the cell bodies of the upper motor neurons, referred to as Betz cells.

INTEGRATES ALL EXCITATORY AND INHIBITORY SIGNALS FROM CORTEX AND TRANSLATE IT INTO A SIGNAL THAT INHIBITS OR INITIATES VOLUNTARY MOVEMENT PYRAMIDAL -MEANS THEY TRAVEL TO MEDULLARY PYRAMIDS .

FROM HERE THEY TRAVEL DOWN SPINAL CORD AND LATERAL CORTICOSPINAL TRACT (LCT) TO CONTRALATERAL SIDE

LCT SYNAPSES DIRECTLY ONTO LMN IN ANTERIOR HORN OF SPINAL CORD

PYRAMIDAL FIBERS THAT DID NOT INTERSECT AT MEDULLARY PYRAMID TRAVEL DOWN MUCH SMALLER ANTERIOR CORTICOSPINAL TRACT ( ACT)-

AND ARE REPONSIBLE FOR AXIAL (HEAD TRUNK) AND PROXIMAL LIMB MOVEMENT + CONTROL =POSTURE-THEY INTERSECT AT SPINAL LEVEL BEING INNERVATED

The primary motor cortex is supplied primarily by the middle cerebral artery (MCA), along with the anterior cerebral artery (ACA). The MCA supplies the area of the primary motor cortex that is responsible for the upper limbs and face, while the ACA supplies blood to the area that controls the lower limbs.

AS IT TRAVELS DOWN THE BRAIN AND SPINAL CORD OTHER ARTERIES PROVIDE BLOOD SUPPLY

RESPONSIBLE FOR TRANSMITTING THE SIGNAL FROM THE UPPER MOTOR NEURON TO THE EFFECTOR MUSCLE TO PERFORM A MOVEMENT OR QUICK MUSCLE RESPONSE

3 TYPES of neurons

BRANCHIAL , SOMATIC AND VISCERAL-FOUND IN BRAINSTEM AND SPINAL CORD-ANTERIOR HORN( where umn msynapses w lmn)

SOMATIC -Somatic motor neurons are in the brainstem and further divide into three categories: alpha, beta, and gamma.SKELETAL MUSCLE

somatic:SINGLE AXON FIRES MANY MUSCLES FIBERS FOR SYNCHRONOUS ACTION, FINE TUNE MUSCLE ACTION,AFFECT TONE-dont actually have motor effect.sense a muscle fiber/spindle stretch.A reflex arc allows for interpretation of and reaction on the stimulus immediately through the spinal cord, bypassing the brain, resulting in a faster effector response

CN V, VII IX X AND XI ARE BRANCHIAL LMN INNERVATING HEAD AND NECK-sensory and motor

CN III VII IX AND X ARE VISCERAL 3 PATHWAYS, FIRST TWOSYMPATHETIC(In the sympathetic nervous system, central motor neurons are present in the spinal cord from T1-L2 FIGHT OR FLIGHT AND PARASYMPATHETIC in the spinal cord at levels S2-S4AND INNERVATE ALL ORGANS HEART GANGLIA AND PANCREAS LUNGS KIDNEYS.tHE Third possible pathway in this system is to the catecholamine-producing chromaffin cells of the adrenal medulla.

https://www.ncbi.nlm.nih.gov/books/NBK554616/#:~:text=The%20upper%20and%20lower%20motor,and%20glands%20throughout%20the%20body.

UMN AND LMN SIGNS

SENSATION BOWEL AND BALDDER FUNCTION SPARED

MILD COGNITIVE DYSFUNCTION IN EXECUTIVE FUCNTION TO DEMENTIAD

PSEUDOBULBAR EFFECTS CAUSE EMOTIONAL OUTBURSTS AND LABILITY

LESION ANYWHERE FROM CORTEX TO CST. depending on where the lesion is it can cause:

HYPERREFLEXIA

SPASTICITY

POSITIVE BABINSKI REFLEX-FANNING OUT AND UP OF TOES

or . Negative features include impaired motor control, easy fatiguability, weakness, and loss of dexterity.

LMN LESIONS ARE Anywhere from the anterior horn of the spinal cord, peripheral nerve, neuromuscular junction, or muscle.

Distinct lower motor neuron lesion findings will include hyporeflexia, flaccid paralysis, fasciculations, and atrophy.  

FASCICULATIONS-FOCAL MULTIFOCAL OR DIFFUSE

FLACCID PARALYSIS

HYPOREFLEXIA

ATROPHY

MAINLY IN LCT THIS PATHYWAY INTERSECTS AT MEDULLARY PYRAMIDS:

THEREFORE:

ABOVE THE PYRAMID IS CONTRALATERAL

BELOW THE PYRAMID IS IPSILATERAL. explanation:

Focusing mainly on the lateral corticospinal tract, it is essential to keep in mind that this neuronal pathway decussates/intersects at the level of the pyramids in the medulla. This crossing means that an upper motor neuron lesion above the medulla will cause symptoms on the contralateral side of the body. However, a lesion to the lateral corticospinal tract after it decussates will present on the ipsilateral side of the body.

Upper motor neuron syndrome occurs when there is injury anywhere to the descending tract before the anterior horn of the spinal cord (cortex, internal capsule, pyramidal tract, lateral corticospinal tract).

UMN: STROKE, TBI, SCI, ALS , MD , PRIMARY LATERAL SCLEROSIS AND ANOXIC BI

LMN: ALS ,SPINAL MUSCULAR ATROPHY, KENNEDY DX-BULBAR ATROPHY,

POLIO -FLACCID PARALYIS -WEST NILE VIRUS, COCKSACKIE,ALL DESTROY ANTERIOR HORN CELL

FASCICULATIONS ARE LMN

While most cranial nerves are innervated by upper motor neurons bilaterally, cranial nerves VII and XII are the exceptions, as they receive only unilateral input from the contralateral side of the brain

age 55—70

male> female

caucasian>

5 in 100,000

5-10% familial

genetic defect C9orf72

cause unknown

excess glutamate accumulation in cns and abnormal mitochondria theory

impaired axonal structure or transports theory

SOD1 enzyme function altered by free oxygen radicals

Evidence that oxidative stress plays a role in initiation of the disease

Summary

Upper and lower motor neurons

Both somatic motor and branchiomotor nerves supply voluntary muscles. Pathways between motor cortex and muscles may be thought of as being arranged in two neuronal groups: upper motor neurons and lower motor neurons. Axons of upper motor neurons decussate before synapsing with lower motor neurons, so the right motor cortex controls the left side of the body, and vice versa – contralateral control.

Upper motor neurons: cortex to nucleus

For cranial nerves, cell bodies of upper motor neurons are in the head and neck area of the motor cortex. Axons descend, decussating just before synapsing with cell bodies of lower motor neurons which make up the motor nucleus of that cranial nerve. The term upper motor neurons is also used clinically to include fibres from other brain centres (e.g. parietal lobe, basal ganglia, cerebellum, reticular formation, midbrain, etc.) that connect with the lower motor neurons in the cranial nerve nucleus, thus influencing their activity.

Lower motor neurons: nucleus to muscle

Cell bodies of lower motor neurons form the brain stem nucleus. Axons leave the brain stem and pass in the cranial nerve to the destination. Thus, although most of the axon of the lower motor neuron is part of the peripheral nervous system, the cell body and first part of the axon is in the central nervous system.

Corticonuclear and corticobulbar

These terms describe the upper motor neuron pathways described above.

There are many forms of motor neuron disease, the most common of which is amyotrophic lateral sclerosis (ALS). This disease is unique in that it presents with both upper and motor neuron signs. The patient will typically present with weakness, along with spastic paralysis and hyperreflexia in the lower limbs and flaccid paralysis and hyporeflexia in the upper limbs. The patient may also present with fasciculations in both the tongue and extremities. Of note, there is no sensory loss. ALS is a progressive neurogenerative disease, and eventually, the patient will have serious dysarthria, dysphagia, extreme weakness, and dyspnea. The estimated median survival is 2 to 4 years, with the most common cause of death being respiratory failure.[

LABS

CMP

ESR

TSH

B12

CK

LFT

SERUM PROTEIN AND IMMUNOFIXATION ELECTROPHORESIS

CSF CULTURE

IMAGING:

MRI HEAD AND CERVICAL SPINE

EMG

LUMBAR PUNCTURE

SPONDYLOTIC CERVICAL MYELOPATHY

KENNEDY DISEASE ( TREMORS ORAL FASCICULATIONS AND LOWER LIMB WEAK -LMN)

MOTOR NEUROPATHY

RILUZOLE

ANTIGLUTAMATE( SLOW EXCITATION)

MONITOR FOR >LFTS AND NEUTROPENIA Q 3 MONTHS

EDAVARONE

FREE RADICAL SCAVENGER REDUCES OXIDATIVE STRESS

INFUSION

SSRI/SNRI- FOR DEPRESSION, PSEUDOBULBAR EFFECTS

SARI -TRAZODONE TO SLEEP

BENZODIAZEPINES,

ANTICHOLINERGICS: TCAS,GLYCOPYRRALATE(LAMA GLYCOPHYRIUM), ATROPINE-FOR DROOLING(SIALORRHEA)

BOTOX-DROOLING

TIZANIDINE (ALPHA ADRENERGIC AGONIST) OR BACLOFEN FOR SPASTICITY

NUEDEXTA- EMOTIONAL LABILITY FROM PSEUDOBULBAR AFFECT

OXYBUTININ ( ANTICHOLINERGIC)-URGENCY

PAIN MGT

NSAIDS, OPIOIDS GABAPENTIN STEROIDS

PHYSICAL THERAPY

SUPPORT GROUPS

RD -MALNUTRITION RISK

DEVICES, HOME CARE, POLST, VENTILATOR

LIFE EXPECTANCY 3-5 YEARS, UP TO 20 YEARS

SURVIVAL FACTORS: BULBAR SYMPTOMS AT DX AND AGE

Afferent neurons are sensory neurons that carry nerve impulses from sensory stimuli towards the central nervous system and brain, while efferent neurons are motor neurons that carry neural impulses away from the central nervous systme and towards muscles to cause movement.

SMALL 20-100,000 ANNUAL

AGE 15-45

M=W

3RD TRIMESTER PREGNANCT OR 1ST WEEK AFTER GIVING BIRTH

CN VII- AFFERENT -FROM TONGUE AND EXTERNAL AUDITORY CANAL

EFFERENT TO FACIAL MUSCLES

PARASYMPATHETIC TO LACRIMAL SUBLINGUAL AND SUBMANDIBULAR GLANDS

EXPLANATION:

While most cranial nerves are innervated by upper motor neurons bilaterally, cranial nerves VII and XII are the exceptions, as they receive only unilateral input from the contralateral side of the brain. Specifically, damage to the corticobulbar tract and/or facial nerve causes a unique presentation depending on whether the damage occurred in the upper vs. lower motor neuron. The forehead region is dually innervated by corticobulbar tracts from each side of the brain, while the rest of the face below the forehead is innervated primarily by the lower motor neuron of CN VII. An upper motor neuron lesion of the facial nerve can occur anywhere in the corticobulbar tract rostral to the facial motor nucleus on the pons. If an upper motor neuron lesion occurs, the forehead will be spared due to its dual innervation. However, a lower motor neuron lesion of CN VII results in flaccid paralysis of the entire ipsilateral side of the face.[14]

IF UMN STROKE THEN CRANIAL NERVE V11 WILL BE INTACT,SO INNERVATED?

SUDDEN TEMPRARY WEAKNESS, HALFFACE INCLUDING FOREHEAD ( PERIPHERAL NERVE V11)

SMILE ONE SIDED,

CANNOT CLOSE ONE EYE, PALPEBRAL FISSURE

OCCURS ANY AGE

EXACT CAUSE UNKNOWN

LASTS FEW WEEKS TO6 MONTHS

RARE PERMANENT

A) Normal anatomic landmarks during smiling and raising the eyebrows. B) On the left, the nasolabial fold is flat and the mouth is turned down but the forehead wrinkles are intact and the palpebral fissures are symmetric. C) On the left, the nasolabial fold is flat, the mouth is turned down, the forehead is not wrinkled and the palpebral fissure is widened. Illustration Brook Wainwright Designs

IDIOPATHIC

VIRAL

HSV 1 & 2

CMV

ADENOVIRUS

MUMPS

COXSACHIE

HZV

HIV

FLU

LYME

AUTOIMMUNE

GUILLAN BARRE

FLU B

DIABETES

AFFECTED SIDE IPSILATERAL NERVE

SMOOTH FOREHEAD

WIDENED PALPEBRAL FISSURE

INABILITY TO CLOSE EYE

CHANGE IN SALIVA/TEAR PRODUCTION

DOWNWARD DROOPING MOUTH

NASOLABIAL FOLD FLATTENED

DROOLING

MILD HEARING DEFICIT

ALTERED TASTE

POSTAURICULAR PAIN

SENSITIVE HEARING

NUMBNESS CN V TRIGEMINAL

REMEMBER CRANIAL NERVE 5 (TRIGEMINAL ) IS SENSATION OF FACE

CRANIAL NERVE V11 IS MOTOR FUNCTION AND SENSORY

FACIAL TRAUMA?

RECENT INFECTION

VIRAL CHICKENPOX, MUMPS, MONO, COXSACKIE, CMV, HIV,FLU

PREGNANCY > 3 X+ 3RD TRIMESTER

RECENT SKIN LESIONS RASHES OR INSECT BITES

LOOK IN EAR AROUND EAR, ON FACE FOR VESICLES HZV

ASSESS CN VII - PUFF OUT CHEEKS, SHOW TEETH, RAISE EYEBROWS , CLOSE EYES TIGHTLY

IS FACIAL WEAKNESS LOWER FACE ONLY-FOREHEAD WRINKLING NORMALLY ? THEN SUSPECT A CENTRAL NOT PERIPHERAL NERVOUS SYSTEM -STROKE TUMOR

IS THERE ANY WEAKNESS ANY OTHER PART OF BODY?

HEENT: OTOSCOPY, PALPATE FOR MASSES NECK AND FACE.

MOTOR:

CHECK CNV11 PUFF CHECKS SHOW TEETH RAISE EYEBROWS, PURSE LIPS MOTOR

SENSORY:

ANTERIOR 2/3 TONGUE TASTE, FACE AND EAR SENSATION ( ?V AND V11

SKIN -RASHES

NEURO:

REFLEXES

TAP OBICULARIS REFLEX:TAP GLABELLA AND OBSERVE FOR ASYMMETRY IN BLINK PATTERN

BELL PHENOMENON, OBSERVE UPWARD MOVEMENT OF EYES DURING FORCED EYE CLOSURE

NONE EXCEPT R/O

TEST FOR LYME, HIV, RPR( RAPID PLASMA REAGIN- FOR SYPHILLIS) AND DM

MRI FACIAL NERVE/EAR/FACE-

*ONLY IF ATYICAL SIGNS -

RECURRENT PARALYSIS >3 MONTHS

, ISOLATED PARALYSIS OF ONE BRANCH OF NERVE VII

OR SIGNS OF STROKE!

ELECTRODIAGNOSTIC TESTING- FOR PTS WITH COMPLETE FACIAL PARALYSIS AFTER 7 DAYS

STROKE- UNILATERAL TO OTHER EXTREMIIES

MS-MULTIPLE NEUROLOGICAL SX

TUMOR-GRADUAL ONSET, MENTAL STATUS CHANGE, CANCER HX

GUILLAN BARRE- BILATERAL

SARCOIDOSIS -BILATERAL

LYME- IN ENDEMIC LYME AREA, ARTHRALGIAS

RAMSAY HUNT SYNDROME- HZV OTICUS-PAIN SEVERE, VESICULAR ERUPTION EAR CANAL OR OROPHARYNX

OTITIS MEDIA-FEVER CONDUCTIVE LOSSES, EAR PAIN

CORTICOSTEROIDS WITHIN 72 HOURS

DOSE PREDNISONE OR PREDNISOLONE 60-80 MG FOR 5 DAYS WITH TAPER 10 MG /DAY FOR A TOTAL AT LEAST 10 DAYS!

SOMETIMES COMBINED WITH ANTIVIRAL

NEURAMINIDASE INHIBITOR

ACYCLOVIR 400 MG PO 5 X DAY FOR 5-7 DAYS

VALACYCLOVIR 1000 MG 3 X DAY FOR 5-7 DAYS

alacyclovir is first line due to superior bioavailability and ease of administration HOLLIER

NSAIDS FOR PAIN WHERE APPROPRIATE

TYLENOL

OPTHALMOLOGIST IF CORNEAL ABRASION, OR FAILED EYE PROTECTION- FOR BOTOX OR MORE

PRGEGNANCY-OBSTETRICIAN

ATYPICAL PRESENTATION OR NO RESOLUTION 2 WEEKS - NEUROLOGIST. OTOLARYNGOLOGIST, PLASTICS , NEUROSURGEON FOR BOTOX THERAPY OR FACIAL NERVE GRAFT,DECOMPRESSIVE SX FOR 90% NERVE COMPRESSION

EYE PROTECTION

PROTECTIVE EYEGLASSES

TAPE CLOSED AT NIGHT

UPPER EYELID WEIGHTS

EYE DROPS Q 2 HOURLY ARTIFICIAL TEARS, EYE PROTECTION DAY

TAPE EYELID SHUT, NO PATCH AS EYE REMAINS OPEN, AND EYE LUBRICANT Q NOCTE

EXERCISES

• Raise eyebrows and hold for 10-15 seconds

• Curling and snarling lips

• Wrinkling the nose

• Tilting head and stretching neck

• Smiling

• Actively closing eyes

REFERRALS

SURGICAL DECOMPRESSION CONTROVERSIAL WINDOW DAY7-14 NEUROLOGY

BOTOX INJECTIONSIF NOT RESOLVED 3 MONTHS -OTOLARYNGOLOGIST

PHYSICAL THERAPY TO RESTORE MUSCLE STRENGTH

FACIAL MASSAGE - WARM MOIST COMPRESS

ACUPUNCTURE

BENIGN

SHARED DECISION MAKING

EYE PROTECTION IMPORTANCE

DISCUSS RED FLAGS:

OCULAR PAIN, DISCHARGE OR DRAINAGE,

MED EDUCATION

FACIAL MUSCLE EXERCISES 2-3 X A DAY

80% COMPLETE RECOVERY 6 WEEKS TO 3 MONTHS

15% LONG TERM NERVE DAMAGE

4% SEVERE SEQUELAE-FACIAL ASYMMETRY, VISION LOSS, HEARING LOSS, TINNITUS

ISCHEMIC 85%

HEMORRHAGIC 15%

FEW MINUTES AREA DIES, LACK OF 02 AND FAILURE OF ADENOSINE TRIPHOSPHATE (ATP)

REMEMBER ATP PRODUCTION FROM MITOCHONDRIA -RESPIRATORY LUNGS OF CELLS

MALE,

FEMALE DEATH RATE 60% MALE 40% AA>

HTN

AGE

TOBACCO

FAMILY HISTORY

RACE

PREVIOUS STROKE OT TIA

CAROTID STENOSIS >80%

AFIB

DRUG ABUSE

DM

OBESITY

HLD

NO EXERCISE

THROMBOTIC -ATHEROSCLEROSIS

EMBOLIC-CLOT,EG AFIB

ARTERIAL OCCLUSION - RESISTANCE TO BLOOD FLOW>

VISCOSITY OF BLOOD>

ISCH + HEMORRH SIMILAR

ISCH -SINGLE ATTACK + EVENT OVER FEW HOURS-72 HOURS

SYMPTOMS VARY

CAROTID -OCCURS IN IPSILATERAL EYE OR CONTRALATERAL BODY

AMAUROSIS FUGAX- CLASSIC SIGN, PAINLESS VISION LOSS-CURTAIN OVER EYE

HEMISPHERIC INJURY- WEAK OR NUMB CONTRALATERAL SIDE

LANGUAGE , COGNITIVE, BEHAVIORAL CHANGES

VERTEBROBASILAR ( POSTERIOR BRAIN AT BASILAR ARTERY) -VERTIGO, SEVERE N&V, NYSTAGMUS, DIPLOPIA, DYSCONJUGATE GAZE, CN DEFICITS

OCCUR IN HEALTHY ADULTS 40-60 YO

RISK FACTORS

HTN BIGGEST

SMOKING

HLD

BLOOD THINNERS

FAM HX

OBESITY DM AV MALFORMATIONS

TRAUMA

ANEURYSMS

10-15 %

WORSE PROGNOSOS

ICH 2/2 HTN =PRESSURE ON WALLS WITH ATHEROSCLEROSIS , ANEURYSM OR AV MALFORMATION

PRIMARY ICH 78-88% -SPONTANEOUS RUPTURE 2/2 CHRONIC HTN

SECONDARY ICH: CEREBROVASCULAR ABNORMALITIES, TUMORS , IMPAIRED COAGULATION

SAH

USU FROM ANEURYSM OR AV MALFORMATION

RISK FACTORS FOR SAH

SMOKING

POLYCYSTIC KIDNEY DX

CONNECTIVE TISSUE DISORDERS

TIA

NARROWING OF MAJOR ARTERY 2/2 <BLOOD FLOW-CAROTID

TRAVEL OF EMBOLUS INTO BRAIN FROM SOMEWHERE

PLAQUE ACCUMULATION IN BRAIN ARTERY <BLOOD FLOW

TEMPORARY

WARNING SIGN

ISCHEMIC STROKE

THROMBOTIC- ATHEROSCLEROSIS

EMBOLIC-CLOT PIECE FROM ELSEWHERE

EFFECT OF BLOCKAGE + SEVERITY + LENGTH OF ISCHEMIA+ LOCATION IN BRAIN

SAH

SEVERE SUDDEN HEADACHE-”WORST OF LIFE”

N&V

MENINGEAL IRRITATION ( CONFUSION RASH FEVER ETC)

LOC INITIAL FOR SHORT TIME

REPORT HX OF INCREASINGLY SEVERE HEADACHES

SEIZURES SOMETIMES

BLEED BETWEEN BRAIN AND LAYER OF SUBARACHNOID

BLEEDING DISORDER OR ANEURYSM, OR AV MALFORMATION

TISSUE DIES ,NO O2 NO ADENOSIEN TRIPHOSPHATE ( MITOCHORNDIRA , CELL RESPS ETC)

INTRACELLULAR CA++ RELEASE CONTRIBUTES TO CELL DEATH

ICH- INTRACEREBRAL HEMORRHAGE

BLEED INSIDE BRAIN TISSUE

WEAK ARTERY AND HTN PRIMARY

NO WARNING OR PRODROME

BP ELEVATED

HEADACHE FOLLOWED BY

FACIAL SAG, HEMIPARESIS

PARTIAL FIELD OF VISION LOSS

EYES DEVIATE FROM SIDE OF PARESIS OR AFFECTED LIMBS STRONG SIGN

ADVANCED- COMA , DEEP RESPS, FIXED DILATED, DECEREBRATE RIGIDITY

each quadrant, Dr. Josephson recommended. The goal is to test “if they blink each time it looks like you are about to poke them in the eye.”

“It’s very helpful in confused patients,” he said. “A lot of times, a visual field cut can identify a parietal or temporal lobe lesion that would have otherwise been missed.” He said he records the results of this simple maneuver as “does or doesn’t blink to threat on one side.”

DOLLS EYES

Doll’s eyesA simple test for cranial nerves III and VI is the oculocephalic maneuver, otherwise known as “doll’s eyes.” If the patient is in a coma, move his head to one side. If the eyes gradually drift back toward the midline, that’s a normal response; if the eyes remain deviated out towards the side of the head, this brainstem reflex is absent, suggesting dysfunction of the midbrain and pons. Touching the cornea and eliciting a blink tests cranial nerves V and VII. Gagging, coughing and watching for spontaneous breathing tests cranial nerves IX and X.

ABCD SCORE SUUPOSED TO BE USED TO PREDICT CVA RISK IN FIRST 2 DAYS AFTER TIA- UPTODATE- SUBOPTIMAL SCALE

1-3 POINTS NEURO CONSULT

4POINTS+> HOSPITAL

TIME CRITICAL

ABC-AIRWAY ,BREATH,CIRCULATION

LOOK FOR

PUPILLARY FUNCTION

GAZE DEVIATION,

BLINK TO THREAT NEXT SLIDE

MOTOR TONE

PURPOSEFUL MOVEMENTS

ICH

SBP >220 MMHG

N&v

SEVERE HEADACHE

ER

STAT CT HEAD (GOLD STANDARD FOR ACUTE HEMORRHAGE). NO CONTRAST

EKG

PO2 ABG

NIH STOKE SCALE

ABCD RISK SCALE

LABS

CBC DIFF

PTPTT INR

CMP

TOXIC SCREEN

LUMBAR PUNCTURE

F/U

MRI

CT HEAD W CONTRAST

MRI

CTA

NEURO

SEIZURE

SUBDURAL/EPIDURAL HEMATOMA

SYNCOPE MIGRAINE

TRANSIENT GLOBAL ANEMIA

METABOLIC ENCEPHALOPATHY

CARDIAC

TRANSIENT GLOBAL AMNESIA

ARRHYTHMIA

METABOLIC

HYPOGLYCEMIA

NONKETOTIC HYPEROSMOLAR COMA

PSYCHIATRIC

CONVERSION DISORDER/ FUMCTIONAL MOVEMENT DISORDER

PANIC ATTACK

DRUG OD COCAINE OR AMPHETAMINE

IMMUNOLOGIC

MENINGITIS

INFECTION-SEPSIS

DEMYELINATING DISEASE

ER

NEUROSURGEON -ICH SAH >ICP W NEURO DEFICITS

CAROTID ENDARTERECTOMY ESP W PTS IPSILATERAL DEFICITS

PRIMARY STROKE CENTER- MEASURES TIME FROM ARRIVAL TO ADMINISTERING THROMBOLYTICS

COMPREHENSIVE STROKE CENTTR

NEUROL, NEUROSURGEONS, NEURO ICU, INTERVENTI RADIOLOGISTS

AND(EXTENSIVE REHAB SERVICES ON SITE) WRONG INFO

IV TPA WINDOW 4.5 HOURS

LOTS OF CRITERIA

ANTIPLATELET AGENTS

ASA

PLAVIX

PERSANTINE ( DIPRYDAMOLE)

AGGRENOX

HEPARIN-PROTAMINE SULFATE

VIT K ANTAGONISTS COUMADIN VIT K

DOAC

RIVOROXABAN-XARELTO Fxa NOW ANTIDOTE FOR DOACS

APIXABAN -ELIQUIS fXa

DABITRAGRAN-PRADAXAFII PRAXBIND

TPA WINDOW INCREASED TO 4.5 HOURS

EXCEPT PT ON DOAC, DM, HX OF STROKE AND >80 YEARS OLD

IF ANTIHYPERTENSIVE NEEDED, USE ORAL AGENTS FOR SLOWER REDUCTION, RISK OF DECREASED REPERFUSION

SX

MECHANICAL THROMBECTOMY DAWN TRIAL EFFICACY IN 1ST 24 HOURS-ENDOVASCULAR

CAROTID ENDARTERECTOMY

VENTRICULOSTOMY TO REDUCE ICP

COIL PLACED IN ANEURYSM BY INT RADIOLOGY

MODIFIABLE RISK FACTOR REDUCTION

HTN RX

CIGARETTE/TOBACCO

OBESITY

STRESS

DM

SEDENTARY LIFESTYLE

HLD

EDUCATE S/S

FAST

FACE

ARM

SPEECH

TIME

CALL 911 IMMEDIATELY

REHAB WITHIN 48 HOURS

6TH LEADING CAUSE OF DEATH

CANNOT BE PREVENTED CURED OR SLOWED

50% RESIDENTS IN NURSING HOMES HAVE DEMENTIA

RISK FOR VASCULAR:

SMOKING

DM

HTN

HLD

PVD

2 MOST COMMON:

VASCULAR

ALZHEIMERS

OTHERS

LEWY BODY

TBI RELATED

SUBSTANCE /MEDICATION RELATED

FRONTOTEMPORAL

1.AMYLOID PLAQUES

2.NEUROFIBRILLARY TANGLES

3.MULTIPLE AREAS FOCAL ISCHEMIC CHANGES-LACUNAR INFARCTS CLASSIC

1. LEWY BODY PROTEINS IN BRAIN ENTER NEURONS AND DESTROY THEM, LOSS OF DOPAMINE PRODUCING NEURONS TOO-PARKINSON LIKE

MEMORY LOSS

PERSONALITY CHANGE

LANGUAGE

ADLS

PT USUALLY HAS NO CONCERN OVER FORGETFULNESS

THOSE WHO WORRY ABOUT FORGETTING NAMES CARKEYS USU BENIGN FORGETFULLNESS OR DEPRESSION-IRONIC

LEWY BDY- HALLUCINATIONS PARKINSONS SYMPTOMS

ALZHEIMERS

EARLY TIME AND SPATIAL DISORIENTATION, JUDEGEMENT POOR, DEPRESSION,

MIDDLE-RECENT AND REMOTE MEMORY WORSE, APHASIA HYPERORALITY, PERSEVERATION, IRRITABLE

LATE-I KNOW THESE + IMPAIRED IMMUNE SYSTEM

NEURO EXAM

DETAILED HX FROM FAMILY

SCREENINGS - NOT SUPER RELIABLE

MMSE

KATZ INDEX OF INDEPENDENCE IN ADL

GET UP AND GO NOW TUG TEST

MINI COG

ONLY LABS TO RULE OUT REVERSIBLE CONDITION

CBC

TSH

VIT B12

FOLATE

CMP 14

MED LEVELS IF ON DIGOXIN, DEPAKOTE TEGRETOL, THEOPHYLLINE

BASLINE CT BRAIN

MRI IF ATTTENTIONAL OR FRONTAL TEMPORAL SYNDROMES OR R/O STROKE

CONSIDER DELIRIUM- INFECTION, MI, DRUG TOXICITY

DSD- DELIRIUM IN SETTING OF DEMENTIA IS SIGN OF ACUTE ILLNESS

DELIRIUM IS CLOUD OF CONSCIOUSNESS,

PSEUDODEMENTIA- 2/2 DEPRESSION

W NEURO SIGNS

HUNTINGTONS

DIFFUSE LEWY BODY DX

HIV

WITHOUT

ADRENAL INSUFFICIENCY

LIVER DX

LOW THYROID

CUSHINGS

VIT DEFICIENCY : B12,FOLIC ACID, THIAMINE

VIRAL ENCEPHALOPATHY

SYPHILLIS

ALL SORTS

EXCESS SYNTHESIS AND SECRETION OF THYROID HORMONE BY THYROID GLAND

>T4-FREE THYROXINE

> T3 TRIIODOTHYRINONE

OR BOTH

<LOWERED TSH

CAUSES

GRAVES

IODINE HIGH INTAKE EG POST CONTRAST-IODINE RICH DRUG AMIODARONE-LOW ODDS

HASHITOXICOSIS

RADIATION

PITUITARY GLAND DYSFUNCTION, HASHIMOTOS INITIAL

DRUG INDUCED - LITHIUM, AMIODARONE

SUBCLINICAL D-LOW TSH NORMAL T4

TOXIC MULTINODULAR GOITER (TMNG)

WOMEN 8X >MEN-THYROID DISORDER

1 in 8 WOMEN-A THYROID DISORDER NOT JUST >THY

PREGNANCY -MISCARRIAGES

USU DX 20-40

FAMILY HX ESP MATERNAL

FEMALE SEX

INGESTION OF THYROID REPLACEMENt HORMONE

OTHER AUTOIMMUNE DISORDERS

DOWNS trisomy 21 and graves-children

IODINE DEFICIENCY-usu associ w hypothyroid but can cause diffuse and nodular goiter over time autonomous growth and leads to toxic goiter and hyperthyroidism

hypothyroidism from iodine deficiency is now extremely rare-gove someone too much iodine and they get hyperthyroid

VIRAL INFECTIONS,

STRESS

SMOKING

HYPOTHYROIDSIM ADVERSELY AFFFECTS LIPID METABOLISM

DYSLIPIDEMIA COMMON WIHT TSH >10 MU/L

CHECK TSH IF DYSLIPIDEMIA

HYPOTHYROIDISM CAUSES OTHER LAB ABNORMALITIES:

lO SERUM NA

HI SERUM PROLACTIN

HI SERUM HYMOCYSTEINEMIA

ANEMIA

HI CREATININE PHSOPHOKINASE -THIS IS ck OS

GRAVES CAN CAUSE DIFFUSE GOITER-GRAVES ONLY IN >THYRIDISM

WEIGHT LOSS

INCREASED APPETITE DESPITE WT LOSS

NERVOUS

DYSPNEA

HEAT INTOLERANCE

PALPS AND TACHYCARDIA-AFIB , SYSTOLIC MURMUR, CARDIAC FAILUREOR MYOPATHY AFFECTS LEFT VENTRICULAR FUNCTION

SKIN WARM MOIST FLUSHED

MUTLIPLE BMS OR DIARRHEA

IRRITABILITY

IMPAIRED CONCENTRATION

TREMORS , > DTRS

NO OR FEW PERIODS

MEN ERECTILE DYSFUNCTION

EXOPHALMOS -BULGING EYES WITH REDNESS, VISION CHANGES-BLUR , DIPLOPIA. STARING EYES AND LID LAG

TEST FOR LID LAG: + IF SCLERA SEEN ABOVE IRIS AS PT LOOKS DOWNWARD-DO FINGER MOVEMENT TEST

INFILTRATIVE/GRAVES DERMOPATHY - OVER SHINS RAISED ORANGE PEEL TEXTURE PAPULES

BONE -THYROID HORMONE STIMULATES BONE RESORPTION CORTICAL AND SKELETAL-> OSTEOPOROSIS? RAISES SERUM ALK PHOS AND CA++

ANXIETY

ARRHYTHMIAS

DM 1 AND 2

CANCER

MENOPAUSE

PHEOCHROMOCYTOMA RARE ADRENAL NEOPLASM, GENETIC MUTATION, ABDOMEN 90%

PREGNANCY

DEPRESSION

CARCINOID

LIFE THREATENING

MORTALITY RATE 8-25% STILL ( 2022)

AGITATION

HYPERPYREXIA

TACHYCARDIA-ARRHYTHMIAS-HEART FAILURE

ABDO PAIN AND D+V

COOL

IN MD CALC

MEASURES TEMP

HEART RATE

CNS EFFECTS

HF SIGNS

GI SIGNS

PRECIPITANT HX

LABS

TSH:LO <0.05MIU/L-IF NORMAL THEN R/O HYPERTHYR

T4: INCREASED OR NORMAL

T3 INCREASED OR NORMAL -GREATEST INCREASE W GRAVES

TSH RECEPTOR ANTIBODIES >

THYROID STIMULATING IMMUNOGLOBULIN -TSI : HIGH LEVEL> =GRAVES DX

SUBCLINICAL-LOW TSH + NORMAL T3 T4

SOME CRITICALLY ILL PT W/O HYPER MAY HAVE LOW TSH,BUT USU HAVE LOW T4 T3-RULES IT OUT

TESTS

1.RADIOIODINE UPTAKE SCAN : RADIOACTIVE IODINE

MEASURES HOW MUCH IODINE THE THYROID IS TAKING UP FROM BLOODSTREAM TO MAKE THYROID HORMONE

GRAVES WILL SHOW LARGE THYROID IODINE UPTAKGRAVES-IODINE IN WHOLE THYROID GLAND

NODULES, ONLY SHOWS IN NODULES

1. DOPPLER BLOOD FLOW MEASUREMENTS USS-USED FOR CONTRAINDICATED IODINE UPTAKE TESTS:ALLERGY PREGNANCY BREASTFEEDING

   GRAVES INFERNO- HIGH VASCULARITY IN GLAND

TSH ANTAGONIST FSH ( FOLLICLE STIMULATING HORMONE) AFFECTS FERTILITY

RADIOACTIVE IODINE ABLATION (RAI) 131

THYROIDECTOMY LAST RESORT IF NO REMISSION

REDUCE SYMPTOMS + DECREASE THYROID HORMONE SYNTHESIS

USING ANTITHYROID DRUGS

DO LFT AND CBC BEFORE USING ANTITHYROID DRUGS***

PTU ( PROPYLTHOURACIL) 100-150 MG/DAY DIVIDED Q 8HO MAINTENANCE

START 300-400 MG DAY DIVIDED Q 8 COMES AS GENERIC OR HALYCIL 50 MG TABS ONLY

METHIMAZOLE OR TAPAZOLE 5-20 MG Q8 HR TO START THEN 5-15 PO QD MAINTENANCE ONCE EUTHYROID

)

BETA BLOCKERS - SX MGT PROPANOLOL ATENOLOL

KEEP HR 60-90 BPM

ATTAIN EUTHYROID STATE IN 3-8 WEEKS

• PTU USED AT LOWEST DOSE TO KEEP SERUM T4 AT UPPER LIMIT OF NORMAL

F/U

TSH AND T4 +WBC Q 4-6 WEEKS UNTIL EUTHYROID THEN 3-6 MONTHS

REFER

OPTHALMOLOGY

ENDOCRINOLOGY

ER FOR THYROID STORM

MAJOR DEPRESSION AFTER THYROID UNDER CONTROL - UNMASK OR DAMAGED RELSHIPS DUE TO BEHAVIOR CHANGES

THYROID STORM :SEVERE ANXIETY, FEVER, NAUSEA , VOMITING, ABDOMINAL PAIN, CARDIAC FAILURE

VISUAL DISTURBANCE

MYXEDEMA

THYROID FUNCTION

REGULATED BY THYROID STIMULATING HORMONE -TSH

TSH SECRETED IN ANT PITUITARY GLAND IN RESPONSE TO SECRETION OF THYROTROPIN RELEASING HORMONE -TRH FROM HYPOTHALAMUS

NEGATIVE FEEDBACK LOOP EG

LOW LEVELS OF THYROID HORMONES TRIGGER TRH RELEASE FROM HYPOTHALAMUS.

THIS IN TURN STIMULATES TSH RELEASE FROM PITUITARY.

TSH INCREASES RELEASE OF THYROID ( HORMONES) UNTIL A NORMAL SERUM LEVEL REACHED.

IN THE THYROID GLAND THYROID FUNCTION IS AFFECTED BY GLANDULAR ORGANIC IODINE CONTENT

SYNTHESIS OF T4(THYROXINE) AND T3(TRIIODOTHYRONINE) REQUIRES ADEQUATE QUANTITIES OF IODINE ENTERING THYROID GLAND.

IODINE ENTERS FROM THE BLOODSTREAM AND IS PART OF T3 AND T4

HORMONES ARE TRANSPORTED TO BLOOD STREAM BOUND TO PLASMA PROTEINS .

MOST T4 IS BOUND, FREE T4 IS MEASURED AND REFLECTS THYROID ACTIVITY

80% OF SERUM T3 IS FORMED IN THE LIVER KIDNEY AND MUSCLE FROM DEIODINATION OF T4, REMAINING 2O% FROM THYROID

biceps: C5, C6

Brachioradialis: C5, C6

Triceps: C6, C7

Patellar: L3, L4

Achilles: SI

0 = absent

1+ = hyporeflexia

2+ = normal

3+ = hyperreflexia

4+ and 5+ = abnormally strong contractions with clonus

Finger-to-nose testing—Ask the patient to touch your index finger with his or her index finger, then touch his or her nose repeatedly. Poor coordination of movement indicates dysmetria.

signs of cerebellar - coordination test

Rapid alternating movements—Ask the patient to perform rapid pronation and supination of the hand on his or her thigh or on the examining table.

Heel-to-shin testing—Ask the patient to take the heel of one side and repeatedly move up and down the shin of the opposite leg.

Romberg—Ask the patient to stand with feet together, arms abducted outward with palms up, and eyes closed. Positive Romberg is observed as a swaying motion, or inability to maintain balance, and indicates cerebellar dysfunction.

ORIENTATION

MEMORY -RECENT AND REMOTELUNCH YESTERDAY = ELEM SCHOOL

FUND OF KNOWLEDGE,ASK ABOUT RECENT CURRENT NEWS,PAST HOLIDAY

ATTENTION SPAN- REPEAT BACK 6 NUMBERS< = ADD

CONCENTRATION 100-7 OR 3 WORD 5 MINUTE TEST

LANGUAGE- READ A SENTENCE OR SPELL WORLD BACKWARDS

ABSTRACT- EG MY SISTERS BROTHER IS MY? OR EXPLAIN A PROVERB

OMFACLA

BRUDZINSKI With patient lying on examination table, gently flex the patient’s neck to a chin-to-chest position. The test is positive if the patient attempts to lift legs and flex hips to relieve pain caused by the maneuver.

KERNIGS-With patient resting on examination table, hold leg with hip and knee flexed. Without moving the upper leg, slowly extend the knee, straightening the leg. The test is positive if the maneuver results in pain, with the patient flexing the neck in attempt to relieve the pain.

INJURY-BIOMECHANICAL FORCES-DISRUPTION IN NORMAL BRAIN FUNCTION:

IMPAIRED NEUROTRANSMISSION, LOSS OF ION REGULATION, REDUCED CEREBRAL BLOOD FLOW

FUNCTIONAL RATHER THAN STRUCTURAL DAMAGE

USUALLY SHORT LIVED

USUALLY RESOLVES SPONTANEOUSLY

SYMPTOMS EVOLVE MINUTES TO HOURS

CAN HAVE LOC

CLASS:

MILD

MODERATE

SEVERE

CAN BE OVERLOOKED IN XRAY

DIFFICULTY :

THINKING CLEARLY

RETAINING NEW INFO

FOCUSING

HEADACHE

VISION

NAUSEA VOMITING -EARLY

DIZZY

PHOTOPHOBIA

BALANCE GAIT PROBLEMS

LACK OF ENERGY

EMOTIONAL LABILITY

NERVOUS

PERSONALITY CHANGES

< 30 MINUTES LOC

CONFUSION

BLUNTED AFFECT

PAIN/HEADACHE

DIZZINESS

SLEEP DISTURBANCE

VISUAL DISTURBANCE-SEE STARS , BLURRY VISION, DIPLOPIA

AMNESIA

pRE TRAUMA- ANTEGRADE

POST TRAUMA -RETROGRADE

LOC>30 MINUTES

POST TRAUMA AMNESIA >24 HOURS

SIGNS OF INCREASED ICP:

PERSISTENT VOMITING

WORSENING HEADACHE

INCREASED DISORIENTATION

CHANGING LEVEL OF CONSCIOUSNESS

ABC-NOW CAB

CERVICAL SPINE-STABILIZE IF NEEDED

CHECK LOC, O2 SAT, VITAL SIGNS,

USE CDC ACE QUESTIONNAIRE!!YOU HAV A COPY

GLASGOW COMA SCALE(GCS)

QUICK CHECK EXTREMITIES FOR INJURY, SYMMETRY OF MOVEMENT

QUICK THOROUGH NEURO EXAM

ER

ER

ER

PHYICAL EXAM IS MOST IMPORTANT

ACE QUESTTIONNAIRE

HX OF PRIOR HEAD INJURY

PROTECTIVE EQUIPMENT USED

MECHANISM OF INJURY

VISION

HEARING

RACCOON EYES-SKULL FRACTURE

NECK PAIN

STRENGTH AND SENSATION-LOSS, PARASTHESIAS

BALANCE

DTRS

MEMORY

CONCENTRATION

RECALL

MOTOR

Localizes to pain (Purposeful movements towards painful stimuli; e.g., hand crosses mid-line and gets above clavicle when supra-orbital pressure applied)

1. Flexion/Withdrawal to pain (flexion of elbow, supination of forearm, flexion of wrist when supra-orbital pressure applied ; pulls part of body away when nailbed pinched)

2. Abnormal flexion to pain (flexor posturing: adduction of arm, internal rotation of shoulder, pronation of forearm, flexion of wrist, decorticate response)

3. Extension to pain (extensor posturing: abduction of arm, external rotation of shoulder, supination of forearm, extension of wrist, decerebrate response)

PUPILS

1. Eye opening in response to pain stimulus (a peripheral pain stimulus, such as squeezing the lunula area of the patient’s fingernail is more effective than a central stimulus such as a trapezius squeeze, due to a grimacing effect)

2. VERBAL RESPONSE

1. Inappropriate words (random or exclamatory articulated speech, but no conversational exchange)

2. Confused (the patient responds to questions coherently but there is some disorientation and confusion)

3. MILD 13-15/MOD 9-12/SEVERE 8 OR LESS

https://litfl.com/glasgow-coma-scale-gcs/#:~:text=Localizes%20to%20pain%20(Purposeful%20movements,out%20tongue%20or%20move%20toes)

CT HEAD NO CONTRAST- GOLD STANDARD

CRITERIA

LOC

HEADACHE

VOMITING

>60 YEARS

PHYSICAL EVIDENCE OF TRAUMA ABOVE THE CLAVICLE

POST TRAUMATIC SEIZURE

SHORT TERM MEMORY LOSS

GCS SCORE <15

MRI 2NDARY

PTSD

DEPRESSION

HEADACHE SYNDROME

SEIZURE DISORDER

GENERAL TRAUMA NOT INVOLVING HEAD

FALLS COMMON CAUSE OF TBI

>75 YEARS HIGHEST RATES OF TBI DEATH AND HOSPITAL STAY

IMAGING IF >65 EVEN IN ABSENCE OF LOC

IMAGING FOR ALL PTS ON BLOOD THINNERS WHO HAVE hi

REFER TO SPECIALTYCARE IF NO SX RESOLUTION IN 2-3 WEEKS

IMMEDIATE MEDICAL ATTENITON FOR :

HEADACHE

WEAKNESS

NUMBNESS

<COORDINATION

VISION- UNEQUAL PUPILS

CONVULSION/SEIZURE

> CONFUSION, RESTLESS, AGITATION

**CLEARANCE TO RETURN TO SCHOOL- GIVEN ONCE PT CAN CONCENTRATE 35-45 MINUTES- ADJUSTMENTS SHOULD BE PROVIDED

** CLEARANCE TO PLAY SPORTS GIVEN ONCE ASYMPTOMATIC FOR 24 HOURS W NO MEDS

HELMETS

MOUTH GUARDS

SEATBELTS

CDC HEADS UP CAMPAIGN FOR YOUTH AND ATHLETES

ELDERLY FALL REDUCTION

REMOVE THROW RUGS/CLUTTER

ADEQUATE LIGHTING

INSTALL GRAB BARS, HAND RAILS

WALKING AIDS

ADEQUATE FOOT WEAR

HISTORY

IMPORTANT

NEED RELIABLE HISTORIAN PRESENT

TEMP: ASK IF THEY HAVE TROUBLE DETECTING WATER TEMP

FINE TOUCH DISCRIMINATION- TROUBLE PULLING CORRECT COIN OR OBJECT OUT OF POCKET ( OR GIVE THEM A KEY, PAPAERCLIP

POSITION SENSE, TROUBLE DIFFERENTIATING CAR PEDALS

MENTAL STATUS.

TEST ORIENTATION TO TIME PERSON PLACE

ONE COMPLEX COMMAND

CRANIAL NERVES:

VISUAL FIELDS ONE EYE, PUPILLARY RESPONSES BOTH EYYES, EYE MOVEMENTS IN ALL DIRECTIONS, FACIAL STRENGTH AND HEARING TO FINGER RUB

MOTOR

TEST TRENGTH IN THESE MUSCLES BILATERAL : DELTOID TRICEPS , HAND INTEROSSI, ILIOPSOAS, HAMSTRINGS , ANKLE DORSIFLEX, TEST PRONATOR DRIFT, FINGER TAP, FINGER TO NOSE , HEEL KNEE SHIN, TANDEM GAIT AND WALKING ON HEELS

REFLEXES

PLANTAR, BICEPS TRICEPS PATELLAR AND ANKLE REFLEXES BILATERL( NO BRACHIORADIALIS

SENSATION

TEST LIGHT TOUCH ALL 4 EXTREMITIES , VIBRATION SENSE GREAT TOES

LOC ( AROUSAL) IS PT ALERT OR SLEEPY, IF SLEEPY CANNOT DO MENTAL STATUS

ATTENTION/CONCENTRATION _ ATTENTION IS ABILITY TO FOCUS AND DIRECT COGNITIVE PROCESSES AND RESIST DISTRACTION

CONCENTRATION IS ABILITY TO SUSTAIN ATTENTION OVER A PERIOD OF TIME.

INTERVIEW- OT UNABLE TO FOCUS, DISTRACTED BY OTHER STIMULI, RAMBLES, LOSE TRAIN OF THOUGHT.

DIGIT SPAN FORWARD TEST-RECITE SOME DIGITS AT RATE OF ONE/SEC

PT REPEATS BACK IN SAME ORDER, INCREASE TO 7 DIGITS

NORMAL FORWARD SPAN IS 7 DIGITS -/+ 2- HIGH SENS + SPEC

OTHER TESTS ARE 7 FROM 100, WORLD BACKWARDS, MONTHS OF YEAR IN REVERSE-NOT SPECIFIC

MEMORY

THREE WORDS, 5-10 MINUTE RECALL-RECENT MEMORY

REMOTE

PRESIDENTS BACKWARDS, IMPORTANT HISTORICAL EVENTS, POPULAR TV SHOWS, PERSONAL IF INDEPENDENT VERIFIER PRESENT

POOR MEMORY- WHITE MATTER DAMAGE, KORSAKOFF SYNDROME ( ETOH) CONFABULATE, FRONTAL LOBE DAMAGE

LANGUAGE

FUENCY,LISTEN FOR GRAMMAR, RATE, EASE OF PRODUCTION. ASKED TO GENERATE AS MANY WORDS AS POSSIBLE IN SHORT SPACE OF TIME, EG ANIMALS, F WORDS. CUT OFF 12 FOR ANIMALS, 10 FOR F WORDS-CATEGORY FLUENCY IS TEMPORAL LOBE DAMAGE, LETTER FLUENCY IS FRONTAL LOBE DAMAGE

CONTENT LANGUAGE ERRORS- LOOK UPTODATE

COMPREHENSION- START ONE COMMAND , MOVE TO 3, READ AND WRITE A SINGLE SENTENCE

VISUOSPATIAL

PTS WITH DIFF LOSE THINGS, GET LOST,HAE DIFFICULTY NAVIGATIING EVEN FAMILIAR TERRAIN, VISUOSPATIAL NEGLECT IS CVA. ? BRAIN DYSFUNCTION IN NON DOMINANT PARIETAL LOBE

PRAXIS

FOLLOW COMMANDS-FOLD PAPER INHALF PUT IT IN ENVELOPE

EXECUTIVE FUNCTIONING

PRE FRONTAL CORTEX

IMPAIRED INSIGHT AND JUDGEMENT ARE EARLY SIGNS

EG DIFFICULY W EVERYDAY ACTIVITIES > COGNITIE DEIFICTS

WORKING MEMORY TESTS AS THEY ARE MORE COMPLEX DRAW ON EXECUTIVE FUNCTIONING, EG 100- 7S

STROOP TEST

MOOD AND THOUGHT CONTENT

ASK FAMILY MEMBERS

DEPRESSION-WITHDRAWN AFFECT, COG IMPAIRMENT, POOR EYE CONTACT, TEARFULNESS, OR EMOTIONAL BLUNTING

APATHY AND DEPRESSION ARE DIFFERENT

PSUEDOBULBAR PALSY- TEARFULNESS/LAUGHTER ARE DISPROPORTIONATE, TBI , MS EUPHORIA CAN MASK DEPRESSION

THOUGHT CONTENT- ABNORMAL INTRUSIONS, PERSEVERATIONS, DELUSIONS HALLUCINATIONS ,MOOD AND BEHAVIOR CAN BE CAPTURED IN SCREENS BECK DEPRESSION, NEUROPSYCHIATRIC INVENTORY

MMSE, moca MORE SENSITIVE TO MILD COGNITIVE IMPAIRMENT

II PERIPHERAL FIELDS

ii AND iii PUPILLARY

LOWER LIGHT

PENLIGHT ON BRIDGE OF NOSE, SEE PUPILS EQUAL, RIGHT, DIRECT AND CONSENSUAL, LEFT SAME, THEN “SWING” BETWEEN TWO BACK AND FORTH

PUPIL SIZE SHOULD BE CONSTANT, IF PUPILS LARGER WHEN DIRECTED AT ONE EYE THAN THE OTHERR = AFFERENT PUPILLARY DEFECT, ANTERIOR VISUAL PATHWAY DEFICIT

ii,iv,vi

CARIDNAL SIGNS, LOOK FOR NYSTAGMUS, DIPLOPIA REPORT

CN V

MUSCLES OF MASTICATION, CHIN SIDE TO SIDE

CN viii HEARING, FFINGER RUB , VESTIBULAR FUNCTION LOOK FOR NYSTAGMUS, GAIT AND BALANCE

IX AND X, SAY AAAHSEE IF PALATE SIDES MOVE SYMMETRICALLY

CN IX,X,XII DYSARTHRIA -MOTOR FUNCTION FOR SPEECH PRODUCTION IMPAIRED , NOT A LANGUAGE DISORDER

CNV

LARGEST AND MOST COMPLEX NERVE, CONTAINS SENSORY AND SENSORY FIBERS

OPTHALMIC BRANCH

SENSORY INFO FROM SCALP, FOREHEAD, UPPER EYELID, CONJUNCTIVA, CORNEA, NOSE ,NASAL MUCOSA, FRONTAL SINUSES + SOME MENINGES-DURA AND BLOOD VESSELS

MAXILLARY BRANCH

LOWER EYELID, CHEEK NARES UPPER LIP, UPPERTEETH, GUMS , NASAL MUCOSA, PALATE , ROOF OF PHARYNX, ROOF OF PHARYNX, OTHER SINUSES MENINGES

MANDIBULAR BRANCH

LOWER LIP, LOWER TEETH, GUMS CHIN JAW, EXTERNAL EAR PARTS, MENINGES

PRIMARY

ARTERY OR VEIN CONTACTS TGN AT BASE OF BRAIN, VASCULAR COMPRESSON

SECONDARY

MS, ACOUSTIC NEUROMA, TRAUMA, MENINGIOMA, CYST, SACCULAR ANEURYSM,

MS DEMYELINATION- ECTOPIC IMPULSE GENERATION CAUSES ADJACENT NERVE FIBERS TO HAVE AN EXCHAANGE OF IONS, TRNSMITS IMPULSE, CALLED EPHAPTIC TRANSMISSION

HAS BEEN DESCRIBED AS MOST EXCRUCIATION PAIN IN HISTORY

LASTS UP TO 15 MINS

BURNING STABBING ELECTRIC SHOCK

TRIGGER- LIGHT TOUCH , MAKE UP , BRUSH TEETH, SMILE

USUALLY UNILATERAL

IF BILATERAL SUSPECT MS!

HEAD

NECK

CRANIAL NERVES

EXAMINE EARS,

TEETH MOUTH- POSSIBLE CUASES OF FACIAL PAIN

FINDING OF TRIGGER ZONES SUPPORTS TN DX

OFTEN NORMAL EXAM

FROM H& P

CRITERIA

LASTS > 15 MINS W/O RADIATION

PAIN AT LEAST 3 EVENTS

TRIGGER

ABSENCE OF NEURO DEFICITS

IMAGING

CT OR MRI IF SECONDARY TN SUSPECTED

NEURO REFERRAL

CLUSTER HEADACHE- CLUSTERR LASTS LONGER, WAKE FROM SLEEP

DENTAL - LOCALISED , RELATED TO HOT OR COLD

GIANT CELL ARTERITIS- PERSISTENT PAIN , BILATERAL JAW CLAUDICATION

GLOSSO PHARYNGEAL NEURALGIA- PAIN IN TONGUE, MOUTH OR THROAT FROM SWALLOWING

INTRACRANIAL TUMORS - OTHER NEURO CHANGES

MIGRAINE- LASTS LONGER, NAUSEA, OTHER SYMPTOMS

OTITIS MEDIA- LOCALIZED TO AFFECTED EAR, TYMPANIC MEMBRANE ABNORMAL

POSTHERPETIC ENURALGIA- CONTINUOUS PAIN AND VESICLES FACE OR EAR CANAL

SINUSITIS- PERSISTENT PAIN AND NASAL SX

TMJ SYNDROME- LOCAL TENDERNSSS, JAW ABNORMALITY , PERSISTENT PAIN

TRIGMINAL NEUROPATHY- PERSISTENT PAIN, SENSORY LOSS ASSOC.

INITIAL

ANTICONVULSANTS

CARBAMAZEPINE 100-200 MG BID, INREASE TO MAX 1200 MG DAILY

SECOND AGENT

BACLOFEN,

LAMICTAL

PHENYTOIN

GABAPENTIN( OFF LABEL)

AVOID TRIGGERS

SURGICAL DECOMPRESSION- CRANIOTOMY AND VASCULAR SEPARATION

***SURGICAL ABLATION- MORE POPULAR.

LESIONING OF TRIGEMINAL GANGLION BY RADIO FREQUENCY THERMOREGULATION

NERVE BLOCK- CAN GET MUSCLE WEAKNESS, LOSS OF SENSATION, RECURRENT NEURALGIA

RECURRENCE IS COMMON,

CAN GET EPISODES LONG TIME, MONTHS THEN REMISSION

COMPS FROM PHARM TREATMENT D

4 CHARACTERISTICS

RESTING TREMOR

BRADYKINESIA (SLOWNESS OF MOVEMENT AND SPEED )

RIGIDITY

POSTURAL INSTABILITY

2ND MOST COMMON AFTER ALZHEIMERS

> MEN MEN OVER 60

>50 YAS

MULTIFACTORIAL

GENETIC MUTATIONS

ASSIGNED A PARK NAME

RRK2, PARK7, PINK1, PRKN, or SNCA gene,23 GENES CURRENTLY

IDIOPATHIC

ONLY 10-15% FAMILY HISTORY

WEIRD ETIOLOGY

INVERSE RELATIONSHIP TO PARKINSONS-CIGARETTE SMOKING +

CAFFEINE

REDUCES PD RISK, ADENOSINE A2A RECEPTOR ANTAGONIST

2 8 OZ CUPS A DAY IS CONSIDERED NORMAL/SAF FOR ANYONE

Caffeine is a potent antagonist of central and peripheral nervous system adenosine receptors, thereby stimulating the release of excitatory neurotransmitters [21]. The behavioral effects of caffeine are attributed to its effects on adenosine receptors

PESTICIDES

INCREASED RISK OF PD OLDER AGE

ONSET ASYMMETRIC IN UPPER EXTREMITY

SLOW, TREMORS RIGIDITY

EARLY

ANOSMIA

DROOLING

CONSTIPATION, GI PROBLEMS

RESTLESS LEG SYNDROME

MASK LIKE FACIAL EXPRESSION

BRADYKINESIA

TREMOR AT REST

RIGIDITY- INCL COGWHEEL

BLINKING LESS THAN USUAL

DYSPHAGIA

UNSTABLE POSTURE OR GAIT

4 CARDINAL SIGNS

2 MUST BE PRESENT

TREMOR

BRADYKINESIA

POSTURAL INSTABILITY-LATER IN DX PROCESS

RIGIDITY

LARYNGEAL DYSFUNCTTION

AUTONOMIC DYSFUNCTION- ORHTOSTATIC HYPOTENSION, IMPAIRED INTESTINAL MOTILITY

LEWY BODY DEMENTIA

ESSENTIAL TREMORS

ALZHEIMERS

CLINICAL DIAGNOSIS

2 OF 4

TREMOR

BRADYKINESIA

RIGIDITY

GAIT INSTABILITY

• RESPONSE TO LEVODOPA’

MRI-ONLY TO R/O STRUCTURAL EG TUMOR STROKE

DAT SCAN-DOPAMINE TRANSPORTER SCAN-DOPAMINE VIUSALIZED IN BRAIN-DIFFERENTIATES PARK FROM ESSENTIAL

BUT…NEG EST DOESNT R/OPARKINSONS COS MAY BE EARLY STAGE

POS…CAN BE OTHER RARER THINGS

FIRST

SINEMET-CARDBIDOPA MAKES DOPAMINE CONVERT IN BRAIN ONLY

SECOND-

NONERGOT DOPAMINE AGONISTS

PRAMIPREXOLE, ROPINEROLE, ROTIGOTINE

THIRD-

MAOB INHIBITORS

SELEGILINE RASAGILINE

FOURTH-

ANTICHOLINERGIC

AMANTIDINE OR COGENTIN

DOPAMINE AGONIST

USED W LEVODOPA

PRAMIPEXOLE/MIRAPEX

APOMORPHINE/APOKYN

ROPINEROLE/REQUIP

MAO-B INHIBITOS

ALLOW DOPAMINE IN BRAIN TO ACCUMULATE IN SURVIVING NERVE CELLS

SELEGILINE/XELAPAR

RASAGILINE/AZILECT

END STAGE

SUPPORT GROUPS

WWW.APDAPARKINSON.ORG

https://parkinsonsbuddynetwork.michaeljfox.org/v2/

EXERCISE

PT/OT

TAI CHI

DANCE THERAPY

ST

NUTRITIONAL:

A high-fiber diet, adequate hydration, and regular exercise help manage the constipation of PD.

●Large, high-fat meals that slow gastric emptying and interfere with medication absorption should be avoided.

●The MIND diet may delay the onset and reduce the incidence and progression of parkinsonism. AND DEMENTIA

DEEP BRAIN STIMULATION-IMPLANTED ELECTRODE IN CHESTDD -BLOCKS MOTOR SYMPTOMS GLOBUS PALLIDUS-NOT GREAT

EPISODIC SEVERE HEADACHE WITH NAUSEA AND LIGHT/SOUND SENSITIVITY

GENETIC2019 Global Burden of Disease study found migraine to be second only to low back pain in causing years lived with disability.

FEMALE>MALE

WHITE , BLACK , N/AMER> ASIANS

WORK TIME LOST

OFTEN ACCOMPANIED BY

ANXIETY

DEPRESSION,

INSOMNIA

STRESS

GI DISTURBANCES

ANGINA

HYPOTHALAMUS-PREMONITORY(? PRODROME) ACTIVATION AND SX RX: TARGET FOR NEUROMODULATION

UPPER CERVICAL NERVES- PAIN TRANSMISSION OR SENSITIZATION

RX: TARGET FOR HYPOTHALAMIC PEPTIDES AND MODULATORS

CORTEX

CORTICAL SPREADING - SELF PROPAGATING WAVEOF NEURONAL AND GLIAL DEPOLARIZATION THAT SPREADS ACROSS THE CEREBRAL CORTEX, CAUSING AURAS, INFLAMMATION, CHANGES IN PERMEABILITY OF THE BLOOD BRAIN BARRIER. RX: TARGET FOR NEUROMODULATION

TRIGEMINOCERVICAL COMPLEX-PAIN TRANSMISSION OR SENSITIZATION,HEAD AND NECK PAIN.RX: TARGET FOR MEDS AND NEUROMODULATION

CNS AND PNS INVOLVED

MULTIPLE SOURCES OR SITES OF ACTION

RX: TARGET FOR SMALL MOLECULE ANTAGONISTS AND ANTIBODIES

PAIN TRIVIALIZED BY PROVIDERS

STIGMA-DO NOT SEEK HELP

CLINICIANS- NOT CONFIDENT TO DIAGNOSE

INCORRECT DIAGNOSES

HISTORY IMPORTANT

PIN:

P- PHOTOPHOBIA

INCAPACITY

NAUSEA

FUNDOSCOPY + PUPIL ASSESSMENT

AUSCULTATION OF CAROTID AND VERTEBRAL ARTERIES'

PALPATION OF TEMPORAL ARTERIES

MENTAL STATUS EXAM

EXAMINE FOR NECK STIFFNESS , FOCAL WEAKNESS AND GAIT

DTRS

VITAL SIGNS

FEMALE

MENSTRUAL /HORMONAL CHANGES

ESTROGEN REPLACEMENT

3 X HIGHER IN WOMEN

WHITE PEOPLE

EARLY ADULTHOOD TO MIDDLE ADULTHOOD

RARE AFTER 50

2 OR MORE ATTACKS OF FOLLOWING:

1 OR >AURA-FULLY REVERSIBLE ,VISUAL( 90%) SCOTOMA, SCINTILLATIONS, SENSORY-PARASTHESIAS HAND OR FACE , SPEECH.MOTOR , TINNITUS,

ONE AURA SX SPREADS OVER 5 MIN

>2 OCCUR IN SUCCESSION

LAST 5-60 MINUTES

> 1 SX IS UNILATERAL

>1 IS POSITIVE??

WITH OR FOLLOWED BY HEADACHE

The ID MigraineTM is a simplified diagnostic criteria that has been validated as an effective screening tool for migraine headaches. A patient is diagnosed with migraine if they have had 2 or more of the following symptoms in the past 3 months:

light sensitivity with headache

nausea with headache,

decreased ability to function with headache.

The simplicity of this tool may improve migraine recognition and diagnosis in the primary care setting.14

OR PIN

PHOTOPHOBIA

INABILITY TOFUNCTION

NAUSEA

TWO TYPES

MENSTRUAL MIGRAINE MM

2 DAYS BEFORE TO 3 DAYS AFTER MENSES

WITH OR WITHOUT AURA

MENSTRUAL RELATED MIGRAINE MSM

SAME ONSET BUT CAN ALSO OCCUR LATER IN CYCLE

AT LEAST 2 OF EVERY 3 CYCLES

LASTS LONGER

SOUNDS ALL SAME TO ME

OCCUR ON >15 DAYS/MON FOR 3 MONTHS

5 OR > ATTACKS FILLING CRITERIA FOR W OR W/O AURA

FULFILL ANY OF FOLLOWING ON >8 D/MONTH FOR > 3 MONTHS:

MIGRAINE W AURA CRITERIA

MIGRAINE W/O AURA CRITERIA

RELIEVED BY TRIPTAN OR ERGOT DERIVATIVE

• Systemic involvement (eg, fever, weight loss, cancer, HIV)

• Neurologic symptoms or abnormal neurologic examination

• Onset: new or changed in a patient more than 50 years of age; posttraumatic

• Onset: sudden, peaking quickly (“thunderclap” presentation)

• Papilledema;

• Pulsatile tinnitus;

• Precipitated by movement;

• Positional exacerbation or relief

LUPMA+ 1 MIGRAINE

TENSION

BILATERAL NOT PULSATING, MILDER , NOT AGG BY ROUTINE ACTIVITY

NO N/V/P/P

SLEEP: CONSISTENT SCHEDULE

EXERCISE: CAN BE TRIGGER, BUT REG EXERCISE CAN < MIGRAINES

EAT: AND HYDRATE. DELAYED.MISSED MEALS TRIGGER M, SOFT CHEESES, CHOC, ARTIFICAIL SWEETENERS, ALCOHOL, RED WINE,ONLY 2 COFFEES DAILY

DIARY: KEEP HEADACHE DIARY- FOR DX CHRONIC AND RX

STRESS: TRIGGER, RELIEF CAN BE TRIGGER TOO ( LET DOWN HEADACHE)-MEDITATION AND YOGA HELP, CBT

ACRONYM FOR SEEDS

NO TRIPTANS W UNCONTROLLED HTN

TRIPTANS FIRST LINE, USE CGRPR ANTAGONISTS IF TRIPTANS FAIL

ZAVEGAPANT NEW, NASAL SPRAY NO FDA APPROVAL

ARB BB NEUROLEPTICS ORAL

RECS: USE TOPAMAX FIRST , THEN RIMEGAPANT

BOTOX GOOD FOR CHRONIC MIGRAINE ONLY

TOPAMAX 25 MG - INCREASE TO 50 MG OD OVER A MONTH

30% and 50% of patients with chronic headaches have medication-overuse headache

PLAN

WITHDRAW EXCESS MEDS

BOTOX

ANTI-CGRP MAB

CGRP IS A PRO INFLAMMATORY VASODILATORY NEUROPEPTIDE

NEED TO INHIBIT

NEUROMODUATION, REN DEVICE, USE AS SOON AS HEADACHE COMING ON

5-HT RECEPT AGONIST LASMIDITAN MAKES YOU SLEEPY

PRIMARY

EPISODIC -

2 CLUSTER PHASES

LAST 7 DAYS TO 1 YEAR

CLUSTER FREE >33 MONTHS

CHRONIC

NO REMISSION

OR REMISSION <3 MONTHS

SUDDEN ONSET

LASTS 15 MINUTES TO 3 HOURS

SEVERE PAIN

BORING LANCINATING

UNILATERAL: ORBITAL (EYE), ABOVE EYE, TEMPORAL

ONE RED EYE

ONE STUFFY NOSTRIL

FACIAL SWEATING

SWELLING OR DROOPING EYE

5 OR MORE ATTACKS

HHOLLIER GROUPING OF HEADACHES OVER SEVERAL WEEKS

TRIGEMINAL AUTONOMIC CEPHALALGIA

HTN

ALLERGEN

AV MALFORMATION

CLOSED ANGLE GLAUCOMA ACUTE

HZV

GIANT CELL ARTERITIS

TGN

R/O OTHERS

ESR

TSH

FSH AND LUTEINIZING HORMONE???

CT BRAIN

POLYSOMONOGRAPHY

ABORTIVE

OXYGEN

10L/MIN -15 L/MIN

NON REBREATHER MASK

USE FOR 15 MINUTES

TRIPTANS

IMITREX SUMATRIPTAN

LIDOCAINE 1 ML 4% INTRANASALLY

PREDNISONE

CGRPR ANTI MABS

GALCANEZUMAB

AVOID TRIGGERS

OCCIPITAL NERVE BLOCKS

CBT

THERMALBIOFEEDBACK

ANXIETY

POSTURE

DEPRESSION

W> MEN

RARE OVER 50

BILATERAL

VICE LIKE

FRONTAL OCCIPITAL

INTERMITTENT OR ALL DAY

PALPABLE MUSCLE TIGHTNESS

NO PRODROME

NEGATIVE EXAM NEURO , VS

PAIN ASSOC W NECK FLEXION

ASA

IBUPROFEN

TORADOL 15 ,30 OR 45 MG TORADOL NOW BANNED, KETOROLAC

FIORICET- BUTALBITAL TYLEONL CAFFEINE

FLORINAL- ASP BULBIT CAFFEINE

THUNDERCLAP _ SAH

NECK PAIN W HORNER SYNDROME OR NEURO SIGNS

AMS AND FEVER= INFECTION IN CNS?

FOCAL NEURO SYMPTOMS + PAPILLEDEMA+ N+ V= ICP>

PREGNANT? PRE ECLAMPSIA ( MIGRAINE IN PREGNANCY USU < 2ND +3RD SEMESTER

VISUAL DISTURBANCE + ACUTE CLOSED ANLGE GLAUCOMA, OR WORSE

Circle of Willis

•

Anterior communicating

artery (18%)

•

Middle Cerebral Artery (35%)

•

Internal Carotid Artery (42%)

•

“Posterior Circulation” (<10%

ANYONE

CONNECTIVE TISSUE DISORDERS

FAMILY HISTORY

LOCATION

MCA

INTERNALCAROTID

RARER POSTERIOR

>7 MM

POSTERIOR CIRCULATION

FEMALLE

TOBACCO

HTN

THESE ARE RISK FACTOR FOR YOUR ANEURYSM TO BLEED

NEUROSURGEON

USU DISCOVERED ACCIDENTALLY ON

MRI

FAM HX, 1ST DEGREE RELATIVE DOUBLES RISK DONT ROUTINELY SCREEN

HEREDITARY SYNDROMES ( ? CONNECTIVE DISORDERS)

PRIOR ANEURYSM RUPTURE SCREEN FOR 10 YEARS I GUESS YEARLY

FAMILIAL:

RUPTURE AT SMALLER SIZE AND YOUNGER AGE

TEND TO HAVE MULTIPLE ANEURYSM

2 OR MORE FIRST DEGREE RELATIVE W ANEURYSM- SCREEN

HEREDITARY SNYDROMES-AUTOSOMAL DOMINANT PCKD( POLYCYSTIC KIDNEY DISEASE) SCREEN

EHLERS DANLOS, BICUSPID AORTIC VALVE, FAMILIAL HYPOALDOSTERONISM

PTOSIS, DILATED PUPIL, DOWN AND OUT POSITIONING

ASAP ER R/O POSTERIOR ANEURYSM

MRA-NO CONTRAST, TAKES A WHILE , 15 MINUTES FLAT

CTA, REQUIRES CONTRAST, TAKES 2 MINS

WITHIN 6 HOURS CT HEAD IS 100% SENSITIVE + SPECIFIC

FIRST TREAT HYDROCEPHALUS - PLACE EXTERNAL VENTRICULAR DRAIN-EVD,

MANAGE BP KEEP IT LOW

REPEAT ANGIOGRAM/ DO

THEN SX :

CRANIOTOMY CLP OR EMBOLIZE-PREFERRED

POST -OBSERVE FOR VASOSPASM 3 WEEKS-VASOSPASM CAN CAUSE ISCHEMIA, STROKE

CCB AMLODIPINE, HOURLY NEURO CHECKS

<60 YEARS

>5MM TO AGE 59

>10 MM >0

MICROSURGICAL CLIPPING, OR ENDOVASCULAR EMBOLIZATION

THUNDERCLAP HEADACHE

SEVERE SUDDEN ONSET

WORST HEADACHE OF MY LIFE + ER

NECK PAIN/STIFFNESS

VOMITING

AMS- SIGN OF HYDROCEPHALUS

LOC

APHASIA/STROKE SIGNS

MAY JUST HAVE SENTINAL HEADACHE

TENSION TYPE MOST COMMON

PRIMARY

TENSION

MIGRAINE

CLUSTER

SECONDARY

SIRS

SINUSITIS

NEUROLOGIC

OPTHALMOLOGIC

HORMONAL?

VASODILATION AND CONSTRICTION INFLUENCED BY NEUROCHEMICALS

SEROTONIN 5 HT

DOPMINE

SUBSTANCE P

CGRP