Neurology š§ Flashcards
What is a more specific and sensitive test for CZJ
RT QulC test. Real time quaking induced conversion test
Dx this:
2mo Hx of -
More sleep, withdrawn, cognifitive issues, balance issues, dysmetria, homonymous hemianopia, wide gait. CT ok
CZJ
What is Lennox Gastaut
A seizure disorder. Presents usually below 5. Seizures and learning difficulties. Slow Spike and wave pattern on EEG.
What is miller fisher, and how to Tx
Miller Fisher syndrome (MFS) is a rare neurological disorder that is considered a variant of Guillain-BarrƩ syndrome (GBS). It is characterized by a triad of symptoms, including Ataxia (lack of coordination), Areflexia (absent reflexes), and Ophthalmoplegia (weakness or paralysis of the eye muscles). Tx same as GBS
British Breslin of Guillain Barre āAOOā
Boy falls on toothbrush and then gets hemiplegia and hemianeatstesia. Dx? How to confirm Dx?
Carotid arteryās dissection. Dx with CTA or MRA
Main criteria for thrombectomy
More than 4.5 hours since stroke (means tPA cannot be used). There is large vessel occlusion found on CTA. Neurological dysfunction.
Patient has stroke, less thAn 4.5 hoursā¦ what to do
tPA
Patient has stroke, more than 4.5 hoursā¦. Less than 24. Do what next
Do CTA to check for LVO. If present do thrombectomy
Concussion Managment
Neuro exam, rest 24hrs, lower screen time, grandual return to activity (start with light aerobic stuff). No CT unless alarming signs
These are signs of?
Impact on externally rotated , abducted arm. Now sits in that position. Pain. Shoulder asymmetry. Ancillary fullness.
Anterior shoulder dislocation
List the biggest risk factor for stroke
HTN. Then smoking, then DM, the hyperchol
Mx for familial macrocephaly
Reassure and observe. This is where patient has head circ above 97th percentile. No syndrome, infx, hydrocephalus etc.
Vertigo, unilateral dysmetria, that is sudden onset and persistent. What is the likely cause
Stroke
Mx for FT dementia
Behavioural intervention. Consider SSRIs for overt behaviour
Vascular dementia has prominent deficits in what?
Cognition
What will be seen on a CT and MRI for diffuse axonal injury
CT is often negative. MRI will show grey ā white matter differentiation loss and punctate haemorrhageļæ¼
How can a patient get median nerve palsy from brachial artery cannulation
It can occur due to laceration from the sharp, or compression from a local haematoma. The compression will most likely just be sensory deficit, and reversible. Whereas the laceration will be both motor and sensory deficit
When do we consider prophylactic medication for tension headaches
Is the patient is having more than one headache a month, we consider giving TCA. Obviously stress reduction techniques are important to
Dx this:
Fever, lower motor neurone signs, focal tender back pain, a little slipped disc-like signs.
Epidural abscess
How to Dx and Tx epidural abscess
MRI, and broad spec Abx/aspirate
What stroke signs suggest emboli origin
Sudden and maximal at onset. Many vascular territories can be affected. Risk factors like AF or heart issues.
Dx this:
30 year old. Severe headache. Had Hx of milder episodic right sided headaches. ICP signs.
Ruptured AVM
What can be given to reduce peritumour edema in brainCA
IV GCs
Main Mx of cerebellar haemorrhage.and what are the indications to do this
Surgical decompression, do if Neuro issues, obs hydrocephalus, AMS, BS compressed, more than 3cm hem
Dx this: and Tx:
Young woman, numb in both arms and legs. And weak in arms and legs too. No sensation below neck. MRI shows increase T2 signal in C. Spine, and no masses.
Transverse myelitis. Give IV CS
NEXUS criteria for doing imaging on neck
Neuro issues, intoxicated, tender spine, AMS, obvious injury. Need only 1
If an old person has main difficulty hearing/understanding what someoneās saying, especially in crowded areasā¦ sign of what
Presbycusis. Concinents are high frequency, so this makes it hard to understand people.
diagnostic test for pseudotumour cerebra, and what must be done prior to this
Elevated pressure on LP is diagnostic. But do CT or MRI prior to rule out lesion
Big risk in pseudotumour cerebri. What can be done to prevent
CNII compression and blindness. Other than normal Tx, can do CNII sheath fenestration
Dx this
Agilent has low concentration, poor sleep, fatigue, headaches, dizziness for a month following post concussion.
Post concussion syndrome
How to distinguish thunderclap from SAH and pituitary apoplexy
Apoplexy can affect ACTH and cause drop in BP. CNIII often involved. History of adenoma (headache, lossed libido, mense irregularity),. No neck stiffness like SAH
Adult has new seizure. Tonic clonic. What is the initial Invx aim
Rule out metabolic and toxicological causes. Then can do imaging (MRI in non emergency, CT in emergency)
cephalohematoma presentation and Mx.
At birth. Usually following forcep or vacuum use. Doesnāt cross suture lines. Doesnāt fluctuate. Is firm. Usually self limited
Caput succedanem presentation and Mx
At birth. Boggy and crosses suture lines. Self limited
Subgaleal hemorrhage presentation and Mx
At birth. Emissary veins rupture during delivery . Fluctuating scalp mass that crosses suture line.
Tx of homocysteinuria
B12, B9, B6 and anticoag
Delerium Tx for elderly patient who is agitated
Low dose haloperidol (or atypical if has PD). Bezos CI if elderly
Preventative treatment for migraines in a pregnant lady
BB.
What is the PECARN rule
Paediatric traumatic brain injury, who gets CT. Anyone with RFs; AMS, LOC, big fall, skull fracture signs, vomiting or severe headache
Neurosyphilis Tx
10-14 days of IV penicillin G
Glucocorticoid myopathy (vs other myopathies)
After high dose GCs. esr and CK are normal. There is no pain, just weakness. Whereas statin myopathy causes pain. Hypothyroidism causes weakness and pain. Polymyositis causes weekends, rarely pain. Poly myalgia only pain/stiffness, no weakness, and high ESR.
Signs and symptoms of cryptococcal meningitis
Subacute meningism. High ICP (clogged CSF flow). Immunosurpressed.
CSF of cryptococcosis
Lowish glucose, high protein, lymphocytosis,
Answer this regarding pseudotumour cerebri Tx:
The only disease modifying mx
First line if eye sight not at emergent risk
First line of immediate threat to eye sight
Weight Loss
IV CAI
VP shunt or optic nerve fenestrations
Drugs which can precipitate acute closed angle glaucoma
AntiCh, Decongestant, antiemetics
Type B thoracic dissection often causes damage to which part of the spinal cord.
T10-12. Due to vulnerability to ischemia (adamkeiwicz artery). Dorsal Columns are spared and itās an anterior spinal cord mess!
Describe the whole indication thing for thrombolysis/thrombectomy
They are considered independently. So can do both, either or neither. Less than 4.5 hours for tPA, less than 24hrs for thrombectomy. To do thrombectomy, need proof of large vessel involvement, using CTA
What is usually responsible for central cord syndrome.
Older patients with an underlying cervical spondylosis, get whiplash (over extension of the neck). Causing central cord issue. Lower limbs ok, bladder bowel ok. Sensory loss and weakness in arms and low reflexes
Can we do anticoag or thrombosis in IE induced stroke? And why? What do we do instead?
No, the risk of hemorrhagic transformation is very high, since the infection causes an arteritis. Do IV Abx and removed dodgy valves
Tx for decompression sickness
100% O2, trenedlenberg positioning, IV fluid
What is a breath holding spell. What are the types
Crying, trauma etc. causes a cessation of breathing. This causes cyanosis (Cyanotic types) or just mild pallor (pallid type). Itās 100% normal. There is a risk it comes from IDA, so check
What is tethered cord
Tethered cord is essentially a stretching of the spinal cord. Usually seen in patients with spina bifida, but can also be seen in patient to hyperextend. Usually find progressive gate issues, back pain, continents, lower motor neuron signs, and feet finding such as arched feet and fix flexion of the toes (pes cavus and hammer toe)
What is delayed emergence and emergence delirium after anaesthesia
Emergence delirium is a patient who is hyperactive after general A. Delayed emergence is recovering from general A. Longer than the average patient (30-60 mins). Just rest and reassure, rule out serious issues like stroke.
Anatomy of cephalohematoma and subgaleal hemorrhage
Cephalohematoma is between the periosteum and skull, making it hard and unable to cross lines. Therefore can just observe and be careful of hyperbili when the blood is resorbed. SubG hem is between the periosteum and galea aponeurosis, so it bleeds quick, crosses lines and is fluctuant.
How can diabetes lead to b12 deficiency
Metformin
Cause of diarrhoea following cholecystectomy or bowel resection. If osmotic gap low, and doesnāt stop when fasting
Secretory (bile acid diahhrea)
Is MS flare more likely in preg or post partum
Post partum
What symptoms can precede the focal neuro signs in MS
Fatigue
Which eye issue can be seen in sturg weber
Glaucoma, due to angle deformity
What is paroxysmal SNS hyperactivity
Usually after TBI, the SNS randomly goes into over drive (likely due to damage to centres inhibiting SNS). Often high SNS in times of external stimulation of patient (bathing or repositioning )
Abortive and preventative meds for migraine
Abort: NSAID, triptan, antiemetic, ergot
Prevent: topiramate, amitrypt, beta blocker (Esther, Ashley, Amy)
Causes of TG neuralgia
MS in the pons, mass near the pons, vascular loop compressing TG nerve (most common)
Tremor with these features
Inconsistent
Abrupt onset
Distractable
Chase the tremour
Functional
If a patient has parksinosism and they are on dopamine antagā¦. Whatās the Dx
Drug induced Parkinsonās, so stop the med and the symptoms should go in weeks. Being on a DA antag is a 100% exclusion criteria for ideipathic Parkinsonās.
Febrile seizure Mx
Abort if needed. Tx fever. Reassure and discharge
Patient with subacute CD like signs, and has microcytic anemia, depig areas, fragile hair, edema. After gastric bypass
Cu def
Red flags and exclusion criteria for Parkinsonās
Red flags: early postural instability, early bulbar dysfunction, absent non motor signs, severe orthostasis, symmetry.
Exclusion criteria: PSP, aphasia, anti DA meds, cerebellar signs
Dx this
Low concentration, depression for 6 mo, forgetful and dementia signs. Restless, abrupt facial expression changes, unable to maintain grasp
Huntingtonāsā¦. presents as agitation and restlessness early on
Epidural lidocaine toxicity
Systemic toxicity, can inhibit the inhibitory neurones. Causing perioral numbness, metallic taste, seizures etc.
Concussion Managment
No same day play. Neuro evaluation. Rest for 24 hr. Then start aerobic, to non contact, to contact sports. Low screen time
Nerve supply for the dura. Divide based in anterior/middle, posterior fossi
Nerve supply is from CN V (anterior and middle cranial fossa), CN X (posterior fossa), sympathetics, and C1āC3 cervical nerves.
Is the epidural space deeper or superficial to the dura
Superficial. Just outside the dura, inside the ligamentum flavum.
Cavernous sinus thrombosis involves which CNs
Nerves 4, 5 (2 and 1), 6
CN IV lesion. Head tilts which way
Contra lateral
Nerve responsible for muscles of mastication
CN V
Diplopia worked when walking stairs and readingā¦. CN
IV.
CNV lesionā¦ jaw deviates to which side
Toward
CNX palsy, uvula deviates which way
Away
CNXII palsy, tongue deviates which way
Toward
In terms of facial nerve boundaries (upper face and lower face), which does the eye fall into? Relevance to LMN and UMN thing
Eye and eyelid is upper face, so eye unable to close if itās a LMN lesion only
Central cord syndromeā¦ symptoms and explain them.
Weakness in the upper limbs due to corticospinal loss medially (arms are represented more medially). Also temp and pain loss bilateral, due to caught decussating fibres of the spinothalamic tract (similar to syrinx damage to the anterior commissure).
Main cause of central cord syndrome
Hyperextension of back in elderly, and SC tumours
Other than vascular compression of TG, whatās another common cause of TG neuralgia
MS
If trigeminal neuralgia is bilateral, consider what cause
MS
Left PCA stroke causes alexia or agraphia
Alexia, no agraphia. Cant read, can write
Weber syndrome
Potential from PCA stroke. Causing contra lateral hemiparesis, ipsilatera
CNIII palsy and parkinsonian rigidity
Clumpsy hand syndrome is caused by lesions in which area
Lacunar infarcts
Patient with oropharyngeal injury, gets horners and neck pain/headache
Carotid artery dissection
Most sensitive invx to Dx acute infarct
Diffusion weighted MRI
Common causes of venous sinus thrombosis
uncontrolled infections of central facial skin, the orbit, or nasal sinuse, thrombophilia, trauma
Locked in, vs coma, vs brain dead
What is transcortical motor and sensory aphasia
In true Broca and Wernicke aphasia, repetition is impaired. If repetition is intact, the deficit is called transcortical motor aphasia (TMA) or transcortical sensory aphasia (TSA), and it is caused by a lesion around either the Broca area or the Wernicke area, respectively. Also called secondary aphasia
Difference between transcorticle motor, sensory, wernicke, brocas,
episode of lip smacking associated with an impaired level of consciousness and followed by confusion, Dx?
think complex partial seizures.
If a patient presents with uncontrollable twitching of their thumb and is fully aware of their symptoms, Dx?
think simple partial seizures.
Labrytnhitiz vs vestibular neuritis
Labyrinthitis causes vertigo, Nystagmus and deafness. Where is vestibule neuritis doesnāt cause hearing problemsļæ¼
Lateral pontine/cerebellar stroke vs labrynthitis
Lateral pontine/cerebellar stroke (anterior inferior cerebellar artery territory) may present with similar symptoms but may have additional occipital headache, ataxia, nystagmus, and somatosensory deficits
Lateral medullary/cerebellar stroke vs vestibular neuritis
Lateral medullary/cerebellar stroke (posterior inferior cerebellar artery territory) can present with similar symptoms, but patients have focal findings on exam (ie, ataxia, sensory loss, dysphagia, Horner syndrome).
Complication regarding hearing in merniere (consider frequency)
Patients progressively lose low-frequency hearing over years and may become deaf on the affected side.
When the cause of AMS is not apparent after initial assessment, can we empiric treat for likely causes (eg, WE)
Yes
Pregnancy and post partumā¦ are these risks or protective for MS Flare
pregnancy is protective for MS, but there is an increased risk in the early postpartum period.
When to do LP in MS. Recall Laith chat
If MRI or clinical is equivocal
Steroid dosing for PMR, GCA and GCA with vision loss
PMR only: low-dose oral glucocorticoids (eg,
prednisone 10-20 mg daily)
ā¢ GCA: intermediate- to high-dose oral glucocorticoids (eg, prednisone 40-60 mg daily)
ā¢ GCA with vision loss: pulse high-dose IV glucocorticoids (eg, methylprednisolone 1,000 mg
daily) for 3 days followed by intermediate- to high- dose oral glucocorticoids
How can fistula in dialysis cause ischemia to arm
The vascular steel. See on google
How does dialysis increase B microglob?
The inflam causes increased microglob, but the dialysis machine cannot remove it.
Uremic polyneuropathy is common in patients with ESRD, and causes what signs. Hands or feet more?
causes progressive pain and paresthesia in the feet, not the hands so much
Is the syphilis attack on the SC direct or indirect
Treponema pallium directly damages dorsal sensory roots
Secondary degeneration of the dorsal columns
Signs of cervical myelopathy (the whole axial atlanti subluxation thing
-Neck pain radiating to occipital region
-Slowly progressive spastic quadriparesis
-Painless sensory deficits in hands or feet
ā¢ Respiratory dysfunction (eg, from vertebral artery compression)
What is Hoffman signs
Hoffman sign (flexion and adduction of the thumb when flicking the nail of the
middle finger) suggests a corticospinal tract lesion
Mx for atlantoaxial subluxation
Management involves stiff surgical collars and neurosurgical intervention
What is Critical illness polyneuropathy
complication of sepsis characterized by axonal injury of the peripheral nerves. It is a common cause of weakness after a prolonged stay in an intensive care unit.
Is stroke onset of symptoms usual gradual or sudden
stroke typically occurs acutely with maximum weakness upon presentation
Signs of transverse myelitis
motor and sensory loss below the level of the lesion with bowel and bladder dysfunction. Patients initially have flaccid paralysis (spinal shock), followed by spastic paralysis with hyperreflexia.
Main causes of traumatic carotid artery dissection
Penetrating trauma
ā¢ Fall with object in mouth
(eg, toothbrush, pencil)
ā¢ Neck manipulation (eg, yoga, sports)
Signs of traumatic carotid artery dissection
Gradual-onset hemiplegia
ā¢ Aphasia
ā¢ Neck pain
ā¢ āThunderclapā headache
Invx of choice for traumatic carotid artery dissection
CT or MR angiography
Chiari I
Symptoms sus for pseudotumour cerebri. Order what first
MRI is performed before lumbar puncture to exclude other
causes of elevated IP (eg, space-occupying mass) that would increase the risk of cerebral herniation
Bifrontal ,,migraines are more common in which patient demographic
Children
Does severe AS or other causes of cerebral low perfusion cause vertigo
NO. they cause light headdressā¦.. not the same
Dx the vertigo
Recurrent episodes lasting 20 minutes to several hours
ā¢ Sensorineural hearing loss
Tinnitus &/or feeling of fullness in the ear
merniere
Dx the vertigo
Brief episodes triggered by head movement
ā¢ Dix-Hallpike maneuver causes nystagmus
BPPV
Dx the vertigo
ā¢ Acute, single episode that can last days
Often follows viral syndrome
ā¢ Abnormal head thrust test
Vestibular neuritis. Labyrinthitis if includes deafness
Cephalohematoma Mx
management is with observation. As blood from the cephalohematoma breaks down,
the patient is at increased risk for hyperbilirubinemia and may require phototherapy. cephalohematomas typically resorb spontaneously within a month,
Dx scalp swell
hours after birth with a firm, nontender, nonfluctuant scalp swelling. The swelling is well demarcated and confined to the surface of a single bone because the hematoma does not cross suture lines.
Cephalohematoma
Dx scalp swelling
diffuse, fluctuant scalp swelling that expands after delivery.
Subgaleal hemorrhage
In the prepubertal population pseudotumour cerebri is more headache or vision predominant
In the prepubertal population, headache may be less obvious and vision abnormalities may
be the predominant finding.
Dx this
Limited upward gaze
ā¢ Upper eyelid retraction (Collier sign)
Pupillary abnormalities (ie, reactive to accommodation but not to light)
Parinaud syndrome
When pineal glands cause hydrocephalus, where do they obstruct
aqueduct of Sylvius,
What is a trilateral Rb
trilateral retinoblastoma consists of bilateral retinoblastoma and a pineal gland tumor.
We all know CNIII can be due to Post comm artery berry. What can cause CN IV or VI.
Less commonly, a trochlear (CN IV) or abducens (CN VI) nerve palsy can result from an aneurysm affecting the superior cerebellar or anterior inferior cerebellar artery, respectively.
Severe headache in the setting of CNIII lesion likely indicates what?
Berry aneurysm and SAH
Mx of SAH
Management of a patient with sudden-onset, severe headache should involve head CT scan with angiography to evaluate for active SAH or an enlarging aneurysm with impending rupture.
unilateral headache and ipsilateral Horner syndrome. Dx?
Carotid artery dissection typically
Cluster causes symptoms or parasympathetic signs
Parasymp
Preventions for migraines
Topiramate
ā¢ Divalproex sodium
Tricyclic antidepressants
ā¢ Beta blockers (eg, propranolol)
Abortive for migraines
Triptans (eg, sumatriptan)
ā¢ NSAIDs (eg, naproxen)
ā¢ Acetaminophen
ā¢ Antiemetics (eg, metoclopramide, prochlorperazine)
ā¢ Ergotamines (eg, dihydroergotamine)
Who gets propels for migraines
Have frequent (eg, >4/month) or long-lasting (eg, >12 hours) episodes
ā¢ Experience disabling symptoms that prevent regular activities despite abortive treatment
ā¢ Are unable to take or have had no relief with abortive medications
ā¢ Overuse abortive medication (eg, nonsteroidal anti-inflammatory drugs (NSAIDs]) and have rebound
headache
When to do imaging for headache patients
Neurologic findings: Seizure, changes in consciousness, specific deficits
ā¢ Differences compared to prior headaches: Change in frequency, intensity, characteristics
ā¢ Other: New at age >40, sudden onset, trauma, present on awakening
If the neurologic examination is consistent with brain death, do what to confirm brain death
the patient can be removed from the ventilator for an apnea test. A positive apnea test confirms brain death by documenting an absent respiratory response
Concussion return to play
- Remove from same-day physical play
ā¢ Neurologic evaluation
ā¢ Rest for ā„24 hr
ā¢ Gradual return to normal activity if symptoms do not worsen
ā¢ Physical: light aerobic exercise -āŗ noncontact sports -āŗ contact sports
ā¢ Neurocognitive: limited screen time, school accommodations (eg, frequent breaks
shortened days)
Concussion pathogensis
Pathogenesis involves axonal shearing from rotational acceleration of the brain after a fall or strike to the head.
When to do neuroimaging in concussion
Neuroimaging is not required
for diagnosis but may be performed to exclude structural intracranial injury (eg, contusion, hematoma) in patients
with high-risk features (eg, vomiting, loss of consciousness).
What is second impact syndrome, in relation to concussion
recurrent head injury from any contact sport during the initial recovery
period can lead to second impact syndrome, which is characterized by cerebral edema and can be fatal.
severe traumatic brain injury. Initial head CT scan was unremarkable (eg, no large
hematoma), this presentation is most consistent for what?
diffuse axonal injury (DAI).
Features of benign macroceph. Mx?
Head circumference in 98% percentile And
ā¢ Normal development
ā¢ No syndromic features
ā¢ No signs of increased intracranial pressure (eg, bulging fontanelle)
ā¢ No signs of infection (eg, fever, lethargy)
Reassure that babaaayyyy
Dx of status E (time wise)
ā¢ 5 minutes of generalized convulsive seizure
OR
ā¢ 2 generalized convulsive seizures without interval recovery of
consciousness
Mx of status E
Stabilize circulation, airway & breathing
ā¢ Benzodiazepines (repeat administration until termination of seizure
activity)
ā¢ Begin antiepileptic drugs like Leve
ā¢ EEG monitoring for refractory status epileptics or failure to regain
consciousness
Persistent
unresponsive state, after status E may be due to either:
ā¢ Sedation due to persistent effects of benzodiazepines or
ā¢ ongoing seizure activity without physical manifestations (ie, nonconvulsive status epilepticus).
How to DDx the two?
electroencephalography should be performed.
Did a lil too much benzos for seizing patient. Patient a lil drowsy. Do we flumanezil them?
because of the risk of precipitating
further seizures, sedation related to benzodiazepine use after status is managed with supportive therapy (eg,
securing airway and assisting breathing if necessary) rather than flumazenil.
Appreciate this! Big deal
Restless leg syndrome causes
Iron deficiency anemia
ā¢ Uremia (ESRD, CKD)
ā¢ Diabetes mellitus
ā¢ Multiple sclerosis, Parkinson disease
ā¢ Pregnancy
ā¢ Drugs (eg, antidepressants, metoclopramide)
Pharma two. Drugs for restless leg syndrome
Pramipexole (DA ag), gabapentin. Fe if the cause is iron def
Gabapentin MOA
Gabapenti, has an effect on GABA activity but does not directly target GABA receptors. Actually blocks calcium receptor channels
Tx of malignant hyperthermia
Respiratory/ventilatory support
cessation of causative anesthetic
ā¢ Dantrolene
Neuroleptic malignant syndrome vs malignant hyperthermia. Which is more acute onset
Malig hyperthermiaā¦ usually over minutes.
Chronic inflammatory demyelinating polyneuropathy
Pathophysiology
Clinical findings
Dx
Tx
Pathophysiology
ā¢ Immune-mediated demyelination of peripheral nerves and nerve roots
ā¢ Non-length dependent
Clinical features
ā¢ Progression >8 weeks
ā¢ Motor»_space; sensory
ā¢ Symmetric proximal & distal muscle weakness
ā¢ LMN signs (eg, hyporeflexia, atrophy)
Glucocorticoids
Intravenous immunoglobulin
Plasmapheresis
Dx
CSF: 1 protein, normal white blood cells
ā¢ NCS: decreased conduction velocity (ie, demyelination)
ā¢ Nerve biopsy: segmental demyelination
Likely Dx
both proximal (eg, standing up) and distal (eg, buttoning
shirts) muscles weakened, accompanied by lower motor neuron signs (eg, hyporeflexia, muscle atrophy) and sensation deficits (more motor though). Developed over 10 weeks
Chronic inflam demyelinating polyneurp
In contrast to many other polyneuropathies (eg, diabetic), CIDP is not length dependent. Therefore, it classically causes both proximal (eg, hip girdle) and distal (g, hand) muscle weakness. Symptoms develop over >8 weeks.
CK and ESR levels in
GC myopathy
Myosotis
PMR
HYPOTHYROIDISM MYOPATHY
statin myopathy
GC myopathy Normal, normal
Myositis high, high
PMR normal, high
HYPOTHYROIDISM MYOPATHY high, normal
statin myopathy high, normal
NF2, three things to surveillance
Audiogram
Ophthalmologic evaluation
ā¢ MRI of the brain & spine
What is medication overuse headache
Why do patients generally not get vertigo in schwannoma
Most patients
do not experience vertigo because the tumorās slow growth allows for central compensation of gradual loss of
input.
Dx?
Bilateral motor weakness, classically early flaccid (LMN) progressing to late spastic
(UMN)
Bilateral sensory dysfunction (all somatosensory systems)
Distinct sensory level
ā¢ Autonomic dysfunction (bowel &/or bladder)
Transvers myelitis
Transverse myelitis vs B12 def timing of symptoms
Acute and not acute resp
Tx of vasovagal syncope
Reassurance & avoidance of triggers
ā¢ Counterpressure techniques for recurrent episodes
Brain finding in status Ep
a brain that has seized for >5 minutes is at increased risk of
developing permanent injury due to excitatory cytotoxicity.
Cortical laminar necrosis is the hallmark of prolonged seizures and can lead to persistent neurologic deficits and recurrent seizures.
MG risk factors (mainly meds)
Medications: antibiotics (eg,
fluoroquinolones, aminoglycosides),
neuromuscular blocking agents, cardiac
medications (eg, BBs), MgSOA,
penicillamine
ā¢ Physiologic stress: pregnancy/childbirth,
surgery (especially thymectomy), infection
Tx for MG
AChE inhibitors (eg, pyridostigmine) ā”
immunotherapy (eg, corticosteroids,
azathioprine)
ā¢ Thymectomy
Patients with MG who remain symptomatic despite pyridostigmine therapy generally require
chronic immunosuppressive therapy (eg, corticosteroids, azathioprine), which may induce remission but generally
takes weeks to reach clinical efficacy.
Essential tremor treatment is propranolol, but whatās the second line
Primadone
What is neuropathic tremor,where is it seen
Neuropathic tremor occurs with large-fiber neuropathies (eg, chronic inflammatory demyelinating
polyneuropathy). Although it is also an action tremor that predominantly affects the distal extremities, patients with
neuropathic tremors often show other signs or symptoms of peripheral neuropathy (eg, proprioceptive or sensory
loss, weakness).
Fist invx and Dxic Invx for galactosemia
Supportive laboratory findings on presentation include nonglucose urine reducing
substances suggestive of galactosuria. Absent GALT activity in red blood cells confirms the diagnosis.
Dx this
30 wk gest premat
Seizures or apnea
ā¢ Full fontanelle
Acute anemia
Intraventricular hemorrhage
Premat screening for which thing?
Head US for Intraventricular hem
Any <32 week gest
No screening for NEC or PDA (abd us or echo resp)
Intracerebral hem common locations
basal ganglia (putamen), cerebellar nuclei, thalamus, pons, and cerebral cortex. In order
Gradual onset of symptoms vs acute onset. Which is hemorrhagic and which is Ischemic
Ischemic is acute onset, hemorrhagic is gradual over hiurs
Signs of cerebellar hemorrhageā¦ explain reasoning behind each sign
occipital headache (may radiate to neck/shoulders), neck stiffness (due to extension of blood into the 4th ventricle), nausea/vomiting, and nystagmus. Patients may also have ipsilateral hemiataxia of the trunk (cerebellar vermis) and/or limbs (cerebellar hemispheres)
Worsening limb pain and paresthesia in response to lateral neck flexion is relatively specific for
cervical radiculopathy,
Acute intermittent porphyriaā¦.. neuropathy usually where?ā¦
Peripheral neuropathy most pronounced in the
proximal upper extremities
Can we see autominc signs in acute intermittent porphyria
Yes ā¢ Autonomic dysfunction (eg, tachycardia,
diaphoresis, hypertension)
Tx for AIP
Glucose & hemin (heme analogue)
Name some weird findings seen in acute intermittent porphyria
SIADH, ans dysfunction, urobilingen high,
Please mention the signs of Lesch Nyhan. Including the neuro stuff
Delayed milestones & hypotonia in infancy
ā¢ Early childhood
ā¢ Intellectual disability
ā¢ Extrapyramidal symptoms (eg, dystonia,
chorea)
ā¢ Pyramidal symptoms (eg, spasticity,
hyperreflexia)
ā¢ Self-mutilation
ā¢ Gouty arthritis in late, untreated disease
Which area of the brain is most affected in Lesch Nyhan
Dopaminergic areas. So movement issues ensue, alongside behavioural issues. Then obvs the unic acid stuff
Levels of what can be used to DD. seizure for, pseudo seizure
Serum prolactin levels, which are usually elevated immediately following seizure, are used primarily to
differentiate seizure from pseudoseizure (psychogenic nonepileptic seizure) in adults;
Localising signs after seizure (esp in kids) DDx? And what to do to tell
Toddās paralysis and stroke,,,, so need MRI to tell
Miller Fischer recap
Anti-GQ1b antibodies re
characteristic symptoms of MFS include cerebellar-like ataxia (eg, dysmetria) and areflexia and opthalomoplegia and weakness.
Botulism toxicity
is associated with a symmetric descending weakness ophthalmoplegia may occur, facial
weakness, dysphagia, and dysarthria are typical.
Pathophysiology of syndemans chorea
Molecular mimicry between anti-GAS antibodies & neuronal antigens in basal ganglia
Symptoms of syndemans chorea
- Involuntary, jerky movements (worse while awake & with action)
ā¢ Hypotonia
ā¢ Emotional lability, obsessive-compulsive behaviors
ā¢ ā” Symptoms of acute rheumatic fever
Tx of syndemans chorea
ā¢ Chronic antibiotics (eg, penicillin G)
ā¢ Symptomatic (antidopaminergics [eg, haloperidol])
Does the abnormal movement in chorea continue in sleep?
patientās abnormal, jerky movements that disappear during sleep are consistent with chorea,
First line therapy for
myoclonus;
GABA agonist medication clonazepam (a benzodiazepine) is a first-line treatment
AVM signs and symptoms
recurrent headache, seizure, or focal neurologic deficit (due to compression).if burst can cause SAH or ICH
Mx of FT lobe dementia
No cure, but can give SSRI or atypical antipsychotic for symptoms
How to maintain CPP in TBI. Consider both components
Maintain MAP: isotonic fluids, vasopressor therapy
ā¢ Reduce ICP: head elevation, sedation, osmotic therapy (eg, hypertonic saline,
(= MAP - ICP)
mannitol), decompressive interventions (eg, SF removal, craniectomy)
How to prevent ICH in TBI. One Med we give
ā¢ Antifibrinolytic therapy (ie, tranexamic acid) within first 3 hr. Prevents the local DIC-like reaction (-Kyle)
ā¢ Reversal of preexisting anticoagulation
How to prevent seizure in TBI. Target glucose and BPā¦ how to achieve?
Prevent seizures (eg, levetiracetam, phenytoin)
ā¢ Control blood glucose (eg, insulin to target 140-180 mg/dL glucose)
ā¢ Maintain normothermia (eg, antipyretics, surface-cooling devices)
Signs of Alzheimerās at the beginning
ā¢ Anterograde memory loss (ie, immediate recall affected, distant memories preserved)
ā¢ Visuospatial deficits (eg, lost in own neighborhood)
ā¢ Language difficulties (eg, difficulty finding words)
ā¢ Cognitive impairment with progressive decline
Vascular dementia vs alz starting symptoms. In simple terms
More excec dysfunction in vascular. More memory in alz
Invx for TG neuralgia
MRI/MRA. Conduction studies if cannot do MRI
Why do TMJ disorder patients have morning headaches
Bruxism
4 As of psychoneuro signs of fragile X
ADHD, autism, anxiety, auto canabal (Kyle)
Why is OCP CI in migraine with aura..
These patients are at high risk of Ischemic stroke, so to reduce compound risk, must discontinue OCP
Acute/subacute Herpetic neuralgia Mx
NSAIDs, analgesics
Chronic post Herpetic neuralgia Mx
GabaP, or TCA, or pregabalin
Difference between chorea and athetosis
Athetosis is a slow writhing. Whereas chorea is non rhythmic, brief irregular, unintentional contractions.
Oscillopsia
Feeling of objects moving
Positive head thrust testā¦. Is peripheral or central vertigo
Peripheral
Can CVD risk factor Management decrease the likelihood of alz
Yes, aggressive Mx in midife
Most common psycho issues in Parkinsonās
MDD (up to 20%)
Dementia with Lewy body vs Parkinsonās disease dementia
Parkinsonās disease dementia , Parkinsonās comes first by at least 1 year
Parkinsonās disease dementia Tx for halluc and Tx for dementia elements
Donepizil - dementia
Low dose antipsychotic - halluc
Confusion assessment method for Delerium recquire?
Acute and fluctuating
Inattention
Disorganised thinking or altered consciousness
Patients with Delerium are at increased risk of what, long term?
Cognitive decline
Tx for lambert Eaton. And if that fails
Guanidine. IVIg/CS if refractory
Main invx in sturg weber. The. Some Tx options
Do MRI. laser Tx for port wine stain. Anti epileptic maybe. Check IOP and make sure to keep it normal.
Dx this:
Prolonged (>4 weeks) concussion symptoms after mild TBI:
ā¢ Headache
ā¢ Dizziness
Clinical features
o Sleep disturbance
o Mood changes
ā¢ Cognitive impairment
ā¢ No structural intracranial injury
Post concussion syndrome
Orthostatic tremor
postural tremor considered to be a variant of essential tremor. Orthostatic
tremor occurs in the legs immediately on standing and is relieved by sitting down.
Tremor predominant Parkinsonās. Mx? If young or old
Anti cholinergic, or can do amantadine in older patients to avoid antiCh
MAOI used in what Parkinsonās
Mild conditions
DA agonists ok in young or older patients for Parkinsonās
Younger. Not well tolerated in older
Screening for TS patients (just think of complications and youāll know)
ā¢ Tumor screening
ā¢ Regular skin & eye examinations
ā¢ Serial MRI of the brain & kidney
ā¢ Baseline echocardiography & serial ECG
ā¢ Baseline electroencephalography
ā¢ Neuropsychiatric screening
What is the growth pattern of a cardiac rhabdomyoma
Big in infancy, but regularly regresses itself
List the following in order of most likely to met to the brain. Which two are the multiple nodule causing, and which other causing solitary nodules usually.
Breast
RCC
melanoma
Lung
Colon
Lung, boob, melanoma, colon, rcc
- = multiple
How would imaging be described for neurocysterocosis
Non enhancing, hypodense lesion, calcified granuloma
Mumps triad of symptoms (doesnāt all occur)
Meningitis, orchitis , parotitis
When is CT C. Spine imaging needed in traumatic injury
cervical spine imaging
ā¢ Neurologic deficit
ā¢ Spinal tenderness
ā¢ Altered mental status
ā¢ Intoxication
ā¢ Distracting injury
Best imaging modality for cervical spine
CT!! Not X-ray
The presence of a single vertebral fracture in a patient with blunt trauma is an indication to image what.?
the entire spine. CT scan is the screening modality of choice. ~20% have concomitant fracture elsewhere
How does Cervicle myelopathy cause upper and lower motor neurone symptoms
Cervical myelopathy often causes both spinal cord and spinal nerve root compression, resulting in myelopathic symptoms (eg, upper motor neuron signs below the lesion) and radicular symptoms (eg, lower motor neuron signs, pain in a dermatomal/myotomal pattern). Lhermitte sign (electric shock-like pain with neck flexion) may occur.
Why can face infx cause cavernous sinus thrombosis easily
Because the facial/ophthalmic venous system is valveless, uncontrolled infection of the skin, sinuses, and orbit can spread to the cavernous sinus. Inflammation of the cavernous sinus subsequently results in life-threatening CST and intracranial hypertension.
Unilateral and rapidly becoming BILATERAL CN (3,4,6) signs and headacheā¦. Suggestive of what?
Cavernous sinus thrombosis
Why does edema of the facial area occur in cavernous sinus thrombosis
Veins backlogs and cause hydrostatic edema
New born vs adult botulinum Tx
Newborn= human Ig
Adult= equine anti toxin
Does werdnig Hoffman affect the pupils?
No
Adult botulinum has what prodrome that infant type doesnāt have
Has nausea and vom prior, and diarrhea
Signs to differentiate seizure from orthostaiss
Seizure: post ictal state, auras, tongue bite, incontinence etc.
Orthostasis: rapid return to baseline, preceding light head, pallor or signs of vol depletion
S1 radiculopathy overview
Posterior calf sense gone
ā¢ Achilles reflex goes
ā¢ Sole & lateral foot sense gone
ā¢ Hip extension (gluteus maximus)
ā¢ Foot plantarflexion (gastrocnemius)
Muscles and weakness in L5 radiculopathy
- Foot dorsiflexion & inversion (tibialis anterior)
ā¢ Foot eversion (peroneus)
ā¢ Toe extension (extensor hallucis and digitorum)
Muscles weakened in L2-L4 radiculopathy
ā¢ Hip flexion (iliopsoas)
ā¢ Hip adduction
ā¢ Knee extension (quadriceps)
Which nerve root radiculopathy causes sexual dysfunction and incontinence
S2-24
LP in the setting of potential epidural abcess?.
NO! Can seed into CNS. So do MRI prior
Pseudobulbar vs bulbar palsy. Which is LMN and which is UMN
Bulbar is LMN. Pseudo bulbar is UMN
Thalamus blood supply. Details
PCA and the thalamogeniculate branches
Globes pallidus and hippocampus get the blood supply from which unusual artery
Anterior choroidal
Tx for child mengitis (bacterial and above 1yo)
Vanco, ceph and dexameth (covers strep and neisseria)
Why do we have to do audiological testing after paed bacterial meningitis
Cochlear damage is common. Therefore, because hearing deficits may go unrecognized, all patients with bacterial meningitis should undergo audiologic testing as soon as possible (ideally, before hospital discharge). If left to calcify, cochlear implants are hard to do
Are brain abscess a long term or short term complication of meningitis
Short termā¦. And not common after strep pneumoniae
What are the subtypes of vascular dementia
Early, prominent executive dysfunction in most
Subtypes:
ā¢ Multi-infarct: often with stepwise decline
ā¢ Strategic infarct: associated with localizing cortical deficits (seen often with a noticeable stroke)
ā¢ Subcortical vascular encephalopathy: associated with subcortical signs (eg, urinary
incontinence, gait disturbances)
Difference between strategic infant vascular dementia, and multi infarct vascular dementia
Single, strategic infarction: One infarction may be enough to cause poststroke vascular cognitive
impairment if it affects key brain areas (ie, frontal lobes, thalamus).
ā¢ Multiple infarctions: Multi-infarct dementia occurs when small infarcts combine to cause enough cumulative damage to the brain, resulting in noticeable cognitive deficits. Patients may not have a history of overt stroke but rather have a stepwise decline in cognitive function.
CZDā¦ incub period?
Can be up to 10 years. Obvs once symptoms starts, will kill you in a year
Tx for CZD
Symptomatic treatment only. Nothing to do to slow progresion
Mx overview for pseudotumour cerebri
carbonic anhydrase inhibitors
first-line treatment for idiopathic intracranial hypertension
medication
a loop diuretic can also be added as adjunctive therapy to decreases the rate of CSF production
Operative
optic nerve sheath fenestration
in patients who fail medical management
Mx non pharma for Delerium
Environment:
noise reduction, intervention grouping
ā¢ Sleep facilitation: bright day/dim night lighting
ā¢ Personal interaction: reassurance, physical touch
ā¢ Constant observation: family, professional sitters
ā¢ Mobilization: out of bed, restraint avoidance
Pharma Mx for Delerium
- Pain management: nonopioid when possible
ā¢ Antipsychotics: off-label indication
ā¢ Benzodiazepines: antipsychotic failure/withdrawal syndromes
Why do pyramidal defects cause pronator drift
UMN lesions cause more weakness in supinators > pronators.
Mx of hospital Delerium
Reduce noise, improve room lighting, open window blinds during the day & avoid frequent room changes
ā¢ Constant observation by a familiar person at the bedside, preferably a family member
ā¢ Nonpharmacologic sleep aids for insomnia
ā¢ Early mobilization & minimal use of physical restraints
ā¢ Visual & hearing aids when appropriate
ā¢ Early volume repletion for dehydrated patients
ā¢ Adequate pain control
ā¢ Aggressive chronic disease management (eg, diabetes, COPD)
ā¢ Reduce polypharmacy
ā¢ Monitor & treat for metabolic disturbances, infections & drug toxicity
Likely Dx
progressive ascending paralysis over hours. more pronounced in 1 leg or arm,t. Fever is not present. Sensation is normal. There is no autonomic dysfunction. CSF normal.
Tick induced paralysis
Remove tick and symptoms should improve
Describe the LMN UMN change in anterior SC syndrome
Spine shock, means itās LMN deficit first, then within days it becomes UMN. We obvs have loss of crude touch, pain, temp too.
Explain the cause and presentation of central cord syndrome
Caused usually by hyperextension of neck in Cervicle spondylosis. See image to explain presentation
CNS infections key words:
Photophobia, nuchal rigidity =
Focal neurologic deficits =
Confusion, altered mental status =
CNS infections key words:
Photophobia, nuchal rigidity = meningitis
Focal neurologic deficits = brain abscess
Confusion, altered mental status = encephalitis
We know the three ways people can get brain abcess. Anatomical where do abscesses that form from blood spread form
At gray white matter boundaries.
We know the three ways people can get brain abcess. Anatomical where do abscesses that form from blood spread form
At gray white matter boundaries.
Classic triad for brain abcess
Fever, headache and focal neuro
Describe the age sex epidemiology of M.G.
Age sex dependent. In young women and old men
Meds causing or worsening myasthenic crisis
antibiotics (aminoglycosides recall NMJ tox, fluoroquinolones), hydroxychloroquine, and Ī²-blockers can precipitate crisis
Main way to tell MG vs antimuscarinc tox?
AntiM will have ANSā¦. MG crisis wont
Examples of ANS dysfunction in LES
This results in autonomic dysfunction, including xerostomia, erectile dysfunction, constipation, and impaired pupillary light response.
HLA loci in MS
MS has been associated with the HLA-DRB1 locus
Which MS type has the best Px
Those with a relapsing and
remitting history have the best prognosis.
How to enhance active MS lesions on MRI
Active lesions are enhanced with gadolinium.
Miller Fischer triad AAA
ophthAlmoplegia, Ataxia, and Absent reflexes.
Significance of hyponatremia in GBS
hyponatremia can occur and is a poor Px indicator
Remember that ascending paralysis with normal CSF findings and without autonomic dysfunction is characteristic of tick-borne paralysis, not Guillain-BarrƩ syndrome.
STATEMENT IN FIRST AID YOU TIT
MMSE score from mild to major cognitive disorder
24-27 mild. Less than 24 is major
DUM MUD for Alzheimerās and NPH
Alzheimer (DUM): Dementia (early, short-term memory) > Urinary incontinence > Motor
NPH (MUD): Motor (early, gait ataxia) > Urinary incontinence > Dementia
Difference between Parkinsonās gate and normal pressure hydrocephalus gate
Normal pressure hydrocephalus has preserved arm swinging. Also will not have any tremor
First signs of normal pressure Hydrocephalos
Magnetic gate
What are the good and bad prognostic indicators in normal pressure hydrocephalus
Only motor problems is good, presence of even a mild dementia is
What is the hockey stick sign and which disease is it seen in
It is hyperintensity of the caudate in the puteman , seen in Creutzfeldt Jakob
Pathophys of Huntingtonās
excessive trinucleotide (CAG) repeats on chromosome 4 during spermatogenesis ā abnormally long huntingtin protein ā glutamate excitotoxicity via the NMDA-Rā degeneration of cerebrum + striatum (caudate + putamen) ā loss of gamma-aminobutyric acid (GABA)/ACh, unbalanced dopamine (DA) activity ā triad of motor (chorea), memory (executive dysfunction), and mood (irritability) symptoms.
Restlessness and fidgetiness. Delete the cards. This could be a presentation of an early phase of what movement disorderļæ¼
Huntingtons disease, donāt make my mistake
Pattern of movement issues in Huntingtons disease. Consider early in the disease and late on
Earlier on I have coria, hyperreflexia, urge incontinence. Later on in the disease they become hypokinetic, rigid,, dystonic, dysphasia et cetera
What are some of the pre-clinical Parkinsonās symptoms
Constipation, anosmia, sleep disturbance (rem disorder, restless leg, excess sleepiness) and mood disorders like depression and anxiety. Can pre-date by up to 20 years
Name the loss of neurones/neurotransmitters in each of the following, and the cardinal symptom. Parkinsonās, Alzheimerās, ALS, myasthenia gravis, Huntingtonās
Parkinsonās: loss of doper neurons in the basal ganglia causing extra pyradimal motor symptoms ļæ¼
Alzheimerās disease: loss of cholinergic neurons in the cortex and subcortex causing dementia.
ALS: loss of upper and lower motor neurones.
My senior gravis: loss of acetylcholine receptor function, causing fatigability
Huntingtons disease: loss of Gabba and acetylcholine activity in the cerebrum and straighten. Causing unbalance dopa activity, causing Moto memory and mood signsļæ¼
A couple of things that can help you differentiate ALS from a cervical myelopathy
Symptoms can be similar (UMN and LMN) Generally ALS will have no bladder disturbance and has a normal cervical MRI. Any involvement of cranial nerve tongue or a pharynx suggests pathology above the foreman magnum and this ALS rather than cervicalļæ¼
What is pseudobulbar affect
Honestly what you have. Crying in somewhat sad moments and excessively laughing in mildly amusing moments. Can be seen in any CNS condition, like MS, ALS, Stroke et cetera
What is postural tremor. Versus kinetic tremor
Tremor of hand only when lifted against gravity. Kinetic Tremor is tremble with any voluntary movement
When is postural tremor seen? When is kinetic tremor seen?
Postural scene in physiological tremor and essential tremor
Kinetic is seen in intention tremor and essential tremor
Wilsonās disease main renal complication
Fanconi
MRI findings of VHL
IC calcifications resembling tramline
Sturgeon Weber MRI findings
IC calcifications resembling a tramline
VHL type 1 and 2. Which has risk for phea
Type II
Phae in less than 18 yo. High chance of what?
VHL
Apart from HARP, what else do we see in VHL
Cyst adenoma of pancreas, endolymphatic sac tumour, epididymis cyst
Ataxia telangiectasia
Autosomal recessive disease caused by a mutation in the ATM gene, which encodes DNA repair enzymes. Leads to aberrant repair of double-stranded DNA breaks, causing cell death (eg, Purkinje cells in the cerebellum are particularly susceptible).
Cerebellar ataxia is often the first presenting symptom in infancy or early childhood. Patients may also present with ocular apraxia (inability to control purposeful eye movements), cognitive impairment, extrapyramidal symptoms, and peripheral neuropathy.
Telangiectasias are common, most often in the face, eyes, and ears.
Immune deficiency (especially IgA) predisposes patients to recurrent sinopulmonary
infections, which may lead to interstitial lung disease.
Up to one fourth of patients will develop a malignancy, most often lymphomas or leukemias.
Orthostasis blood pressure defined as?
SBP drop of >20! DBP >10
Tandem gait testing is what?
Heel toe walking
Eye findings in huntingtons
Delayed saccades
Main cognitive impairment domain in HTT
Excec function
Pathophysiology of epidural local anaesthetic systemic toxicity. What are the signs and symptoms
Essentially the needle can release local anaesthetic directly into the epidural vasculature. This will cause inhibition mainly of inhibitory pathways, which causes nerve over stimulation. Patients get perioral numbness, tinnitus, metallic taste in mouth, high blood pressure, tachycardia, and potentially cardiovascular collapse
Describe some of the symptoms of oxytocin toxicity, and the reason behind them
Oxytocin shares similar structure to ADH, causing low sodium, Thos cerebral oedema, seizure
What respiratory changes are seen in Rett syndrome
Tachypnoea and times of low/absent respiratory rate. Due to medullary centre neurones regressing
Abulia
Lack of Will or initiation
Apraxia
Inability to carry out complex motions
Name a couple of signs that you would see in an anterior cerebral artery stroke
Abulia, apraxia, primitive reflexes, emotional disturbance, executive function, flat affect, bladder problems, leg weakness and sensory loss
Clumsy hand syndrome as seen in which kind of stroke
Lacuna
Infant has microcephally, whatās the first thing that you should do. In the case That all of the growth is normal and the patient a stable and developing ok
Measure parents head circumference to assess for family or microcephally. ļæ¼
Tell me some clues that can help differentiate cervical myelopathy from cervical radiculopathy
Myeloprhy is going to cause spinal cord compression. So will cause maybe a few radiculopathy signs, plus upper motor neuron signs, and lower extremity weakness, which is bilateral. Radiculopathy just will cause one side, lower motor neuron, following dermatome patterns usuallyļæ¼
Vertebral body squaring is an early sign of what disease
Ankylosing spondylitis
Symptoms of central venous thrombosis. Dx and Mx?
Headache, ICP signs, seizure sometimes. Can do MRV to Dx. Do anticoag
What kind of stroke can cause unilateral MLF lesion
Pontine from lacunae stroke
Difference between lateral geniculate nucleus and edinger Westphal
Edinger westphal is in the light reflex pathway, whereas LGN is in the normal optic pathway
Medial Lemniscus lesion
Contra loss of vibr proprio and light touch
Signs of post concussion syndrome
Noisy sensitivity, cognitive impairment, dizziness, headache, anxiety, irritability
Most common cause of central cord syndrome
Whiplash type injury (hyperextension of the neck) in an elderly patient with cervical spondylosis.
Signs and symptoms of central called syndrome
That usually happens in the cervical region: upper extremity motor, sensory loss bilaterally. Usually loss of reflexes due to anterior horn involvement. Lower extremities usually spared (recall anatomy of spinal cord)
If you see muscle weakness in almost all the muscles of the body, and maybe a little bit of pain. What should be on your suspicion
An electrolyte problem
List causes of enhanced physiological tremor
Medication such as beta agonists, SSRI, TCA, nicotine, caffeine, steroids. Stress and anxiety. Hypoglycaemia, alcohol/opioid withdrawal, thyrotoxicosis and liver disease
Name all the signs of basil a skull fractures
Raccoon eyes, CSF rhinorrhoea CSF otorhea, postauricular Ekhymosis (a.k.a. Battle sign)
Which neonatal scalp swelling is soft, and boggy and crosses suture lines. But is not life-threatening
Caput succedaneum ļæ¼
Which neonatal scalp swelling is this: present after birth, is firm and non-fluctuant. Does not cross suture lines. Patient is okay. And what is the prognosis
Prognosis is good but there is a hyperbilirubinaemia risk. This is cephalo haematomaļæ¼
Which neonatal scalp swelling is this. Diffuse soft fluctuant expansion over days. Crosses suture line. Can have a bit of bruising overlying it. Patient is someone un stable
Subgaleal haemorrhageļæ¼
Main timing aspect to differential between plagiocephally and neonatal scalp swelling
Neonatal scalp swelling is in neonates. Plagiocephaly is in young infantsļæ¼
Risk factors for sudden infant death syndrome
Maternal substance use, not only is less than 20, inconsistent prenatal care, prematurity or low-birth-weight, prone sleeping position, soft sleep surface, loose bedding, bed sharing, exposure
NMS the lumbar puncture siesta will have high or normal total protein? And high or normal proportion of Ig to rest of protein
Normal total protein, but high immunoglobulin proportion
Investigation of choice for Hydrocephalus in children
CT or MRI. Ultrasound is not as details, and does require a very wide fontanelle to investigate
ļæ¼ Bellās palsy, trigeminal neuralgia. Which is characterised by demyelination/atrophy, and which is characterised by inflammation/oedema
Trigeminal neuralgia is characterised bye demyelination and atrophy. Is Bellās palsy is characterised by oedema/inflammationļæ¼
Wardenburg syndrome, structures affected and subsequent symptoms
Spinothalamic tract, causing sensory loss Contralaterally. Vestibular nuclei causing usual signs. Furious cerebellar peduncle causing ataxia. Nucleus ambiguous causing dysphasia and dysphonia. Trigeminal nuclei causing loss of face at sensationļæ¼
Dissection of the vertebral artery is commonly caused by what kind of trauma?
Rapid expansion of the neck
Intracranial vertebral artery dissection can affect which important arteries
The posterior inferior cerebellar artery, causing Wallenberg syndrome
Only mandatory sign for diagnostics of normal pressure hydrocephalus
Gait.ļæ¼ Incontinent and dementia are not required
Can pseudodementia have an MCA score of the 27
Yes
List some of the neurological complications of sarcoidosis
Cranial nerves! Especially facial nerve palsy. Central diabetes insipidus and other hypogonadotropic hypogonadism.
Does cryptococcal meningitis CSF have normal or low glucose
Low, usually
Likely diagnosis of this. Patient had no headaches for a long time, worse in the morning. Now starting to get weakness on the left side. Cardiovascular risk factors of moderate
Intracranial tumour.
The signs and symptoms of decompression sickness
Respiratory distress, confusion, mottled skin, signs of stroke, especially tingling sensations. Obstructive shock can occur if large coalesced airļæ¼
What is the tetrad for gerstmann syndrome. Where is the lesion
Finger agnosia, right left discrimination, acalculia, Agraphia (writing by hand). This is a lesion on the angular gyrus of the dominant hemisphereļæ¼
Symptoms of lesions in the non-dominant parietal lobe
Heavy neglect, distortion of position sense (feelings of floating) and interpretation of objects (i.e. sighs)
How does facet dislocation present
A single level radiculopathy. Usually seen in the cervicle vertebraļæ¼ļæ¼. Unilateral.
. Usually following forced flexion of the neck
What is shy ā Drager syndrome
Itās a type of multisystem atrophy. Characterised by parkinsonism, Nigel autonomic dysfunction, and potentially other neurological signs like cerebella operatable issues. Usual anti-Parkinson drugs are ineffective and we focus on intravascular volume expansionļæ¼
What is Riley day syndrome
What is a recessive disease in Ashkenazi Jews. Characterised by severe autonomic nervous system problems, including severe orthostasis. Alongside poor muscle tone
Epidural spinal abscess. Classic triad of symptoms, how to diagnose, how to treat
Fever, focal/severe back pain, neurological findings. To diagnose take blood and aspiration cultures, an MRI of the spine. Treat with gold spectrum antibiotics and emergency surgical decompression
What can be used as an alternative to diagnose osteomyelitis, if the patient has contraindication for MRI
Tagged leukocyte scam
MSK findings of NF1
Scoliosis and paeudoarthritis
Three types of cerebral palsy
Spastic, dyskinetic, ataxic
Spastic cerebral palsy symptoms
One or more limbs affected, hypotonia, commando crawling (diplegiaļæ¼) or paraplegia. Contractures and a equinovarus ļæ¼.
Gait type seen in mytonic dystrophy
Waddling
Gait type seen in mytonic dystrophy
Waddling
Papilledema vs glaucomaā¦.. vision loss
Papilledema = large blind spot
Glaucoma = peripheral loss first
How to tell between cyanotic BHS and tet of fallot
Tet of fallot will have hyperventilation. Whereas BHS has breath holdingā¦ā¦ā¦
Dx this
1 year old, falls. Minor. But when lands, stop breathing for a min and becomes limp, LOC and pale
Pallid BHS
Autonomic dysreflexia
Spinal cord full lesion above T6. Anything causing high SNS below lesion (bladder distension from BPH for example) is unaaposed, leading to high SNS neurotransmitter and HTN. The brain will oppose this with PNS, causing flush and low hr
Meds to avoid in MG
Magnesium sulfate
ā¢ Fluoroquinolones, aminoglycosides
ā¢ Neuromuscular blocking agents
ā¢ CNS depressants
ā¢ Muscle relaxants
ā¢ Calcium channel blockers
Beta blockers
ā¢ Opioids
Statins
10 Hz pattern on EEG seen in high seizure
Tonic clonic
Recall our paroxysmal sympathetic nervous system hyperactivity case
After traumatic brain injury the brains centres for SNS can get mixed up. So we get times of increased sympathetic system during times of external stimuli
Dizziness when patient has lots of work out with arms.
Rui heard left clavicle
Subclavian steal syndrome
What is trihexyphenidyl
An anticholinergic. Fairly good for Parkinsonās
Breath holding spell, usually okay, just need to check one thing
For iron deficiency
Point: never forget you remix an catholyte us, looks very similar to hepatic
Which is the curtain across blindness
More retinal detachment, but not 100% sure
Case with history of tripping/falling. Constipation. Microcytic anaemia
Lead poisoning
Cerebella haemorrhage management
Usually surgery, especially if thereās neurological issues, more than 3 cm, brainstem compression, hydro Kefalos.
Five components to the NEXUS To tell us one to do spine cervical imagingļæ¼
Neuro complication, intoxication, obvious injury, tender spine, AMS
