Exam III Flashcards
Primary headaches
not caused by any other disorders – migraine, tension-type, cluster headaches
Secondary headaches
underlying etiology – less serious (withdrawal from caffeine, increase in BP, fever) to serious (brain tumors, strokes, TBI, infections, hemorrhages) – may get resolved if/when underlying cause is treated
Migraine
often familial disorder characterized by recurrent attacks of headache widely variable in intensity, frequency and duration, Hemi-cranial
Associated with nausea, vomiting, sensitivity to light/sound
Migraine triggers
Migraineurs should avoid certain foods. Stress levels, hormone levels, and sleep deprivation are involved. Menstruation, pregnancy, HTN
Auras
prodromal signs – early ‘warning’ signs of migraine
Visual auras, somatosensory or vestibular auras
Feelings of tiredness, excitement, craving for certain foods (chocolate), sometimes auras can be confused as triggers
There may or may not be auras - menstrual migraines occur w/o auras
Hyperexcitation associated with headaches
Headache starts when excitation of cortical or brainstem neurons cross a certain genetically determined threshold – explains auras, but not pain (or throbbing pain)
Migraine w/ Aura
begins with aura, can have visual aura which is temporary visual disturbances. Also can include parathesia, speech difficulty, vertigo/dizziness.
Migraine w/o Aura
No warning signs
headache might be dull or throbbing, may last 4-72 hours, nausea, photophobia, blurred vision, aggravated by routine physical activity
After headache resolves – tender scalp, fatigue, diuresis
Familial Hemiplegic migraine (FHM)
Migraine w/ aura
Aura is paresis with impaired coordination(ataxia), in face, arm, or whole one side of body
Headache could be on contra- or ipsi- side
Differential diagnosis with TIA - no infarction
Basilar-type Migraine
Attack in posterior fossa involving vascular region of basilar artery – brainstem, cerebellum, occipital lobes
Auras could be dysarthria, ataxia, vertigo, diplopia, tinnitus, AMS
Followed by headache
Vestibular migraine – dizziness, nausea, vomiting, motion sensitivity, postural instability, may not have headache
Status Migrainosus
Persists for more than 72 hours
Triggers - Hormonal changes during menstrual cycle, pregnancy, miscarriage, change in birth control pills can be triggers, respiratory and UT infections
Continued vomiting to the point of dehydration, severe headache, may need hospitalization
Migraine treatment
Avoidance of triggering factors
During attack, quiet and dark place is necessary
Pharmacological agents (Triptans, Ergots, CGRP, Botox, NSAIDs)
Triptans
serotonin receptor agonist, stops throbbing pain by constricting cranial vessels, contraindicated with CAD pts, not helpful with auras.
Ergots
relieve severe throbbing pain
Calcitonin Gene-related Peptide (CGRP) receptor antagonist
better pain relief, do not cause vasoconstriction, so safe for CAD pts, also effective with photophobia, phonophobia, nausea
Botox
block peripheral and central sensitization of nociceptive receptors
Tension-Type Headache
most common, episodic TTH is caused by peripheral sensitization of the pericranial myofascial nociceptive afferents
In chronic TTH, there is central sensitization
TTH clinical manifestations
pressure or tightness in whole head, dull and not throbbing, tenderness of tissues around head, increased hardness of muscle in upper cervical area.
Triggers are stress, irregular eating pattern, high coffee intake
TTH diagnosis
Exam should include palpation of pericranial muscles to identify tender and trigger points, specifically in temporal, pterygoid, masseter, SCM, trapezius.
Chronic medication use is associated with TTH, so diagnosis should be made after 15 days free of meds
Cluster Headache
Rare type, but most painful and most disabling type of primary headaches. Increased suicidal thoughts, often in clusters when headache happens daily or several times daily for a period of several weeks.
2 types of cluster headache
2 types – episodic (remission lasts several months) and chronic (remission lasts <14 days)
Cluster headache risk factors
predominantly in males between 27-30 years (black males>). Beer is the most common type of alcohol trigger, other triggers are weather changes and smells
Second hand cigarette smoke exposure during childhood increases risk
Cluster headaches clinical manifestations
Onset is sudden, with excruciating pain, remains always on one side of the head, usually localized to one eye and surrounding frontotemporal region, non-throbbing pain.
During headaches, person prefers to assume erect rather than reclining posture
Attacks occur mostly awakening from afternoon nap or sleep during night, 90minutes after falling asleep.
Cervicogenic headache
secondary headache,
unilateral pain that starts in the neck/base of skull and can come up and around your head to your forehead and behind your eye (ram’s horns)
Can occur as a result of degenerative problems in cervical vertebrae, joints, or neck musclesthat happen over time – secondary to fall, sports injury, whiplash, or arthritis
Cervicogenic headache signs and symptoms
Limited cervical ROM, headache with sudden cervical movement or when neck remains in the same position for extended time (FHP in dentists, carpenters)
Seizure
sudden paroxysmal excessive discharge of cerebral neurons resulting in transient sensory, motor or cognitive impairment
Can happen in normal brains, or secondary to acute conditions
finite event, has a beginning and end
Epilepsy
a chronic neurological disorder, a condition characterized by sudden recurrent episodes of seizures associated with abnormal electrical activity in the brain that manifest as sensory disturbance, motor impairments, loss of consciousness, or convulsions.
“Kindling” phenomenon
neuroplastic phenomenon, Repeated exposure to low-intensity electrical or chemical stimuli results in facilitation/potentiation of connections, leading to seizure activity and increasing severity at later times.
Clinical manifestations of seizures
occur unpredictably w/o any warning signs in most. In others there are prodromal signs (headache, mood, unusual sensations/feelings). In some, seizures are provoked by specific stimuli such as flashing light or a flickering television (triggers)
Generalized tonic-clonic seizure
Classic type, aka grand mal seizure, involves both hemispheres, loss of consciousness.
Starts with generalized rigidity, sustained contractions of limb extensors, arching of back lasting 10-30secs (tonic phase), a cry may be heard due to contraction of chest muscles, may turn blue to due to cyanosis from hypoxia
Followed by generalized rapid jerky movements of limbs (clonic phase)
Followed by period of recovery (post-ictal phase), can last minutes to hours, may feel tired, with headache, confusion, difficulty speaking, may fall into deep sleep with heavy breathing, salivary frothing
Absence seizures
petit mal seizures, generalized seizure, Loss of conscious control, but person is unaware of it. Sudden cessation of ongoing conscious activity, often stares into space. Not preceded by aura, followed by return to normal activity immediately. Occur mostly in children and disappear with adolescence
Focal/partial seizures
Characterized by locus of onset, neuronal activity restricted to a local structure or within networks limited to one hemisphere. EEG shows activity in a focal area.
Symptoms will depend on the lobe the focus is present – frontal lobe (bizarre movements, thrashing of arms, pelvic thrusting, pedaling of legs), temporal lobe (feeling of deja-vu, jamais-vu), parietal lobe (numbness or tingling, agnosia, spatial perceptual distortion), occipital lobe (visual distortions or hallucinations)
Simple partial seizure
Individual retain consciousness, Typically lasts briefly (60-120secs). Individuals get unusual sensations/feelings, altered sense of hearing, smelling, tasting, seeing, tactile perception or involuntary movements. labored speech or inability to speak at all.
May progress to involve additional cortical area ipsilaterally. If somatosensory or motor area are involved, tingling or clonic jerks can progress or ‘march’ from distal to proximal parts (or reverse) known as Jacksonian March.
Myoclonic seizures
Sudden brief single or repetitive muscle contractions involving one body part or entire body, myoclonic jerks. Repeated myoclonic jerks may get severe and turn into generalized tonic-clonic seizures with convulsions
Can happen anytime, but often observed shortly after waking up or while falling asleep.
Complex partial seizures
Dyscognitive seizures
-Loss of consciousness or impairment of awareness or responsiveness
-Often preceded by aura
Once consciousness is lost, may show ‘automatisms’ like lip smacking, chewing, swallowing, may show random walking, pulling at clothes.
May show amnesia about details surrounding event of seizure
Atonic seizures
Aka ‘drop attacks’
Brief loss of consciousness and postural control
Most often in children
Characterized by sudden loss of muscle tone that may result in falls with injury
Sometimes loss of muscle tone happens in neck muscles, causing head drop
Status epilepticus
When person has generalized tonic-clonic seizures that are so long or so repeated that there is no recovery or return of consciousness
Medical emergency, can cause death
Often occurs due to tumor, CNS infection or drug abuse
Febrile seizures in children under 3 years are also a common cause.
4 types of progression with MS
Relapsing-remitting MS (RRMS)
Secondary progressive MS (SPMS)
Primary progressive MS (PPMS)
Progressive relapsing MS (PRMS)
Relapsing-remitting type MS
most common type
Definition of a ‘relapsing attack’ - new symptoms must last at least 24 hours and be separated from other symptoms by at least 30 days to qualify as a new attack.
MS genetic factors
child of MS parent has 5 fold increased risk of developing MS, increased presence of gene for HLA-DR2 (immune system protein) which is responsible for for identifying and binding to foreign molecules.
Families with hx of MS also have other autoimmune diseases – it appears MS develops on a background of increased susceptibility to autoimmune disorders
MS environmental factors
Vitamin D deficiency, Viral infections are also thought to trigger MS – more than 1/3rd relapses are preceded by infections
Pathogenesis of MS
Immune system erroneously attacks myelin basic protein (MBP) in the lipid membrane. Primary pathology is demyelination of CNS nerve fibers
Visual problems associated with MS
Optic neuritis is one of the first manifestations. It typically presents as unilateral painful decrease in vision.
Other ocular problems – gaze palsies, nystagmus, inability to fix gaze – caused by lesions in the pons, vestibular nuclei of brainstem or cerebellum
Fatigue associated with MS
single most common and disabling symptom in MS, often precedes diagnosis by years. Presents as severe tiredness, along with mental fatigue/fuzziness.
Fatigue may not be related to level of effort, unpredictable, tends to be aggravated by heat and humidity
Central fatigue
due to demyelination, nerve fibers start to short-circuit after repetitive firing when called upon to do repetitive task. So, repetitive exercises w/o rest could lead to feeling of increased weakness – should be avoided
Sensory changes associated with MS
Somatosensory symptoms ( hypoesthesia, parasthesia, dysethesia), other sensory losses such as vibration, position, 2 point discrimination.
Symptoms may NOT be substantiated by objective findings, as remission might have happened by the time pt shows up for examination
Weakness or paresis associated with MS
Result of decreased neuromuscular firing secondary to demyelination and axonal loss
Loss of orderly recruitment of motor units
Muscle activation patterns and agonist-antagonist relationships are disturbed
Heat increases weakness – due to conduction block
Cooling improves strength and function
Spasticity associated with MS
Extremely common in MS (UMN lesion), more common in lower extremities. Severity of spasticity can vary from non-existent to severe in same person from to time to time, making it challenging to manage with meds.
Often, MS patients can use their spasticity to walk, transfer and manage ADLs
Cerebellar symptoms associated with MS
Due to cerebellar lesions, axonal loss and/or atrophy
Incoordination, tremor and ataxia – involving the extremities or the trunk
May be symmetric or asymmetric
Dysarthria – scanning speech
Cerebellar signs occur mostly during progressive phases
Balance, coordination and dizziness problems associated with MS
impairments in balance regulating systems, fatigue, body temperature, or from BBPV
Cranial nerve dysfunction associated with MS
When lesions are in brainstem, affecting CN nuclei, can involve CNs III to XII at the nuclei level.
Cognitive problems associated with MS
memory loss, Attention deficits, difficulty in understanding conversations and critical thinking, depression, medications can also cause this.
Pain associated with MS
usually neuropathic type pain, may or may not follow sensory pattern. Fairly constant with nocturnal worsening. Trigeminal neuralgia and Lhermitte sign
Trigeminal neuralgia
shock-like pain in trigeminal’s branches in face, characteristic in young person
Lhermitte sign
momentary electric shock-like sensation evoked by flexing neck or cough. Like other symptoms, more likely to occur when fatigued or overheated
Bladder and bowel symptoms associated with MS
can have urge incontinence, overflow incontinence, or stress incontinence. Also can have bowel incontinence (diarrhea or constipation) but less common
Dissemination in space
showing presence >1 lesions in different CNS regions in an MRI, OR an additional relapse showing new symptoms that implicate another CNS region. For MS, lesions/symptoms required in the MS-typical regions.
Dissemination in time
showing simultaneous presence of active (inflammatory) and inactive (old) lesions in different CNS regions in an MRI scan, done using contrast-enhancing technique using Gadolinium, OR by doing a CSF test (for oligoclonal bands)
DD from ADEM (acute disseminating encephalomyelitis) – acute attack during childhood
inflammatory attack of the brain and spinal cord that damages myelin, with features of encephalitis (fever, headache, seizures and coma) - usually occurs just once, could be the ‘clinically isolated attack’.
Factors that predict worse prognosis
motor and cerebellar symptoms, short time between attacks, numerous attacks within first year or initial years, rapid disability after first attacks
Factors that predict better prognosis
sensory symptoms, infrequent attacks, full recovery after a relapse, low level of disability after 5-7 years of onset
EDSS – 0-3.5
Mild disability
fully ambulatory w/o AD
EDSS – 4-6.5
moderate disability – ambulatory to specific distances w/o or w/ AD
EDSS – 7-9.5
severe disability – very limited ambulation even w/ aid, W/C or bed bound
ALS
Amyotrophic lateral sclerosis, also known as Lou Gehrig’s disease.
Severely progressive neurodegenerative disease that affects nerve cells in the brain and the spinal cord. Adult-onset type of progressive motor neuron disease
Both upper (cortical neurons) and low motor neurons (anterior horn cells) and axons can be affected
Damage/loss of motor neurons lead to profound muscle weakness and wasting/atrophy
ALS Limb onset clinical manifestations
Corticospinal tracts are affected first – limb muscles are affected – 70% cases
ALS Bulbar onset clinical manifestations
cortico-bulbar (brainstem) tracts are affected first - muscles of throat, mouth, face are affected – 25% cases
Initial clinical presentations of ALS
early signs could be trouble grasping a pen/lifting a coffee cup from loss of pincer grip due to APB, FDI weakness – may lead to split-hand sign
Also can be tripping/falls, muscle cramps/twitches, a change in vocal pitch when speaking, and/or uncontrollable periods of laughing or crying (pseudo-bulbar sign). Muscle atrophy, extensors become weaker than flexors
LMN signs in ALS
weakness, muscle wasting (atrophy), muscle fasciculations, cramping
UMN signs in limbs in ALS
spasticity, positive Babinski, exaggerated reflexes, clonus
ALS clinical manifestations
LMN and UMN signs, cervical extensor weakness, weakness followed by deformities. Cognitive impairment in half of cases
In later stages respiratory muscles get affected – accessory breathing replaces diaphragmatic breathing – respiratory distress can occur at night
Sensory functions, eye movements, bladder and bowel functions are mostly preserved
Bulbar signs (LMN-type)
dysarthria, hoarse and whispering voice, nasal tone
difficulty with swallowing, drooling (made worse by forward head position), choking
facial and tongue muscle weakness/low tone - difficulty manipulating food in mouth
Pseudobulbar signs (UMN-type)
known as pseudobulbar palsy – corticobulbar tracts to brainstem are affected – slurred speech, difficulty chewing/swallowing, spastic tongue, uncontrolled emotional outbursts
EMG criteria for ALS
fibrillations, positive waveforms, fasciculations, polyphasic motor unit potentials in at least 3 limbs and paraspinal muscles
Progressive spinal muscular atrophy (PMA)
Only LMN are affected, anterior horn cells of spinal cord affected beginning with cervical area, weakness/wasting of muscles, fasciculations present, can later turn into ALS
Primary lateral sclerosis (PLS)
rarest type of motor neuron disease, only UMN are affected, corticospinal tract involvement, spastic presentation, weakness, increased reflexes, no muscle atrophy, no fasciculations, outcome is less severe compared to ALS (people usually do not die from it), can later turn into ALS
