CNS system Flashcards
What is GCS components?
What to assess in the muscle tone of UL?
How is musle power graded?
What muscles and nerve roots control the shoulder, elbow, wrist and fingers?
What muscles do the median, radial and ulnar nerve control and their action?
What are the reflexes of the UL and their corresponding nerve origin?
What are the sensation landmarks of the upper limb?
How to test for coordination in lower limb
Differentiate between UMN lesion (pyramidal) and cerebellar lesion?
How to assess the muscle tone of the lower limb?
How to assess the muscle power of the lower limb their muscles and corresponding nerve root?
What are the LL reflexes and their nerve origin?
- Knee jerk: L3 – 4
- Ankle jerk: S1 – 2
- Plantar jerk (Babinski’s sign): L5 – S2
What are the sensation landmarks of the lower limb?
How to test the coordination of the lower limb
Loss of proprioception?
How to assess the gait?
What are the functions of CN1-5 and their clinical findings on CN palsy?
What are the functions of CN6-9 and their clinical findings on CN palsy?
What are the functions of CN10-12 and their clinical findings on CN palsy?
How to assess the optic nerve?
- Visual acuity: only 1 eye tested each time. Test with patient wearing his or her spectacles.Refractive errors are not considered to be CN abnormalities
Test with snellens chart at 1 arms length.
If unable to read –> count fingers –> hand movement –> light perception –> no perception of light (blind) - Assessment of pupil size
Physiologic anisocoria: difference <0.4mm
Anisocoria greatest in bright light = larger pupil is affected. Indicates poor pupillary constriction on the abnormal side. Indicates abnormality of parasymp system
Anisocoria greatest in dim light = smaller pupil is affected. Indicates poor pupillary dilatation on the abnormal side. Indicates an abnormality of the symp system
Pupillary light reflex. Direct response: pupillary constriction of the stimulated eye. Consensual response –> pupillary constriction of unstimulated eye
RAPD
Normal RAPD test: relative dilatation of pupil when light shone on the affected eye
Reverse RAPD test performed in patients with unreactive pupils: relative dilatation of the contralateral eye when light shone on the affected eye
ddx of RAPD
Optic nerve: optic neuritis, optic atrophy (glaucoma), ischemic optic neuropathy/compressive or traumatic optic neuropathy
Retina: CRAO/BRAO/CRVO/BRVO/retinal detachment
Accomodation reflex
Light near dissociation is tested by accomodation reflex: accomodate but not react to light
ddx of light near dissociation: argyll robertson pupil (syphilis/DM autonomic neuropathy), Adies tonic pupil
Visual field
What is the function of CN3,4,6 and what is innervated?
Compare medical vs surgical CN3 palsy and its presentation and cause
What is the causes of CN3 palsy based on anatomical location?
Causes of CN4 palsy by laterality
By anatomical location
Causes of CN6 palsy by anatomical location
What to assess in ptosis and the underlying types (ddx)?
How to differentiate the type of diplopia?
What is the pathophysiology of nystagmus
The types, causes and features?
What structure and pathway is involved in the horizontal gaze?
What are the causes of horizontal gaze disturbances?
What are the causes of vertical gaze disturbances?
How to do PE of CNV?
Causes of CNV palsy?
What muscles involved in CN7
What affects UMN and LMN and difference in clinical presentation for UMN and LMN?
How to test the function of CN8 and its results?
What are the causes of conductive deafness (outer ear and middle ear)?
What are the causes of sensorineural deafness ?
How to examine CN9,10 and the causes of these palsies?
How to examine CN11
Causes of CN11 palsy?
How to examine CN12
Causes of CN12 palsy?
Compare bulbar and pseudobulbar palsy in casues, jaw jerk, gag reflex, speech, tongue and emotions
Localization of lesion in the spinal cord?
What is normal range of ICP
What is ICP?
What are the causes of increased ICP?
What regulates cerebral perfusion pressure and cerebral blood flow?
What is the cerebral autoregulation in hypertension?
What are the SS of increased ICP?
What are the cerebral herniation syndromes?
What signs will they have?
What are the indications for ICP monitoring and the method done?
What is general management of increased ICP?
What is the treatment of increased ICP?
Define hydrocephalus
Disorders in which excessive amount of CSF accumulates within cerebral ventricles or subarachnoid spaces which are dilated
How to classify hydrocephalus?
Obstructive (non-communicating) hydrocephalus
* Obstruction in CSF circulation leading to accumulation of CSF in cerebral ventricles
Communicating hydrocephalus
* Impaired absorption of CSF leading to accumulation of CSF in cerebral ventricles
How is the production of CSF and pathway done?
What is the pathogenesis of hydrocephalus?
- Increased CSF production: choroid plexus papilloma
- Decreased CSF absorption: bacterial meningitis (leads to arachnoid granulation adhesions)
- Obstruction of CSF flow: aqueductal stenosis, tumor
What is the clinical manifestation of hydrocephalus?
What is treatment of hydrocephalus?
What are the SS of Horner syndrome?
Interruption of sympathetic nerve pathway to the eye and face
Partial ptosis: Paralysis of Muller’s (superior tarsal) muscle which is innervated by sympathetic pathway and levator palpebrae superioris being unaffected
Miotic reactive pupil: Anisocoria with abnormal small pupil in the dark and associated dilation lag
Enophthalmos: NOT a true enophthalmos and occurs as an illusion due to ptosis and updrawing of lower
eyelid which together narrows the palpebral fissure
Anhidrosis: Loss of sympathetic fibers for facial sweating and vasodilation
What are the causes of Horner syndrome (1st order, 2nd order and 3rd order)?
What is the sympathetic pathway of Horner syndrome?
What are the Ix done to confirm the dx of Horner syndrome?
Define delirium
Acute confusional state characterized by global cognitive dysfunction and inattention
* Confusional state refers to state of altered consciousness with disorder attention along with diminished speed, clarity and coherence of thought
What are the precipitating factors for delirium?
What is the pathophysiology of delirium?
What are the SS of delirium?
What are associated features?
What is the ddx for delirium?
What is the diagnostic criteria for delirium?
DSM-V
What is the history taking for delirium?
What is the PE done for delirium?
What are the basic blood tests done for delirium?
What imagings and non basic Ix may be done for delirium?
What is general management and medical management for delirium?
What are the general features of coma?
Defined by unarousable unresponsiveness
Medical emergency characterized by absence of consciousness
* Consciousness requires arousal (awake) and awareness (have content)
Timely identification and treatment of reversible cause can be life-saving
Caused by structural brain lesions, diffuse neuronal dysfunction or psychiatric illnesses
What are the levels of consiousness?
- Vigilant = Hyperalert
- Normal = Alert
- Lethargy = Drowsiness but easy to arouse
- Stupor = Difficult to arouse
- Coma = Unarousable
What are the tests for certifying brain death?
What is the system involved with consiousness?
Ascending reticular activating system (ARAS)
* Network of neurons originating in the tegmentum of upper pons and midbrain
* Neurons project to thalamus and hypothalamus and subsequently to cerebral cortex
* Responsible to induce and maintain alertness
o Injury to ARAS with upper brainstem or cerebral hemispheres by focal lesions can cause alteration in consciousness
What are the symmetrical structural causes of coma (supratentorial and infratentorial)?
What are the asymmetrical structural causes of coma (supratentorial and infratentorial)?
What are the symmetrical non structural causes of coma?
What are the conditions mistaken for coma?
What initial assessment for coma patient?
What is history taking?
What is done for PE of coma patient?
Must look out for reversible causes and treat promptly
What are the biochemical tests done for coma patients?
What imaging and non blood Ix done for comatose patient?
ABG/ VBG
CXR
ECG
EEG
CT brain
CT angiography
MRI venography
What is the initial stabilization management of comatose patient?
What is supportive care?
What are the red flags of headache in adults?
What is the history taking of headache?
What is the PE for headache?
What is the ddx of headache depending on timeline, patient demographic and associated conditions (i.e. fever, immunocompromised, traumatic brain injury)
What is migraine associated with
Classification of migraine
Precipitating factors of migraine (descending order)
What are the genetics involved in migraine?
What is the pathophysiology of migraine?
What is the clinical manifestation of migraine (4 phases)?
What is the diagnostic criteria for migraine without aura?
ICHD-3
What is the diagnostic criteria for migraine with aura?
ICHD-3
When may imaging be indicated for headache?
What is the treatment for migraine?
What is done for prevention of migraine?
β-blockers
* Propranolol
* Metoprolol
* Timolol
Anti-depressants
* Amitriptyline (TCA)
* Venlafaxine (SNRI)
Anti-convulsants
* Topiramate
* V alproate
What is general feature of tension type headache?
Classification of TTH?
Precipitating factors of TTH?
What is pathophysio of tension type headache?
Peripheral factors
* Peripheral activation or sensitization of myofascial nociceptors
* Associates with pericranial muscle tenderness
Central factors
* Sensitization of pain pathways in CNS due to prolonged nociceptive stimuli from pericranial myofascial tissues
What is clinical manifestatin of tension type headache?
What is the specific PE done?
What is the diagnostic criteria for episodic and chronic TTH?
ICHD-3 (international classification of headache disorders-3rd edition)
What is done for treatment of tension type headache
What prevention management
What is the clinical manifestation of cluster type headache?
What is cluster type headache
What proposed theory for pathophysiology?
Belongs to an idiopathic headache entity known as trigeminal autonomic cephalalgias (TACs)
Severe unilateral headache typically accompanied by autonomic symptoms
Theory 1: Hypothalamic activation with secondary activation of trigeminal-autonomic reflex through a trigeminal-hypothalamic pathway
Theory 2: Neurogenic inflammation of walls of cavernous sinus obliterates venous outflow
* Leads to injury of traversing sympathetic fibers of the intracranial ICA and its branches
What is the diagnostic criteria for episodic cluster headache and chronic cluster headache?
What is treatment and prevention of cluster type headache
What is general feature of trigeminal neuralgia
What is the etiology?
Recurrent brief episodes of unilateral electric shock-like pains that is abrupt in onset and offset
Located in the distribution of one or more divisions of CN V
What is clinical manifestation of trigeminal neuralgia?
What is diagnostic criteria for trigeminal neuralgia?
What radiological Ix may be indicated and why?
What is medical treatment for trigeminal neuralgia
What is surgical treatment (refractory to medical treatment)?
What is giant cell arteritis (temporal arteritis)?
What associated condition?
Is it a medical emergency?
Chronic systemic vasculitis involving large and medium sized arteries: aorta and great vessels. Commonly affects the temporal and other cranial arteries originating from the aortic arch
Strongly associated with polymyalgia rheumatica in 40-60% of patients. Characterized by pain and morning stiffness around shoulder and hip girdles, neck as well as in the torso. However GCA only found in 15% of patients with PMR.
Medical emergency (amourosis fugax) du to cranial arteritis without early detection and treatment
What is epidemiology of giant cell arteritis
RF
Pathogenesis
What is the SS of giant cell arteritis?
What is diagnostic criteria for temporal arteritis (giant cell arteritis)
What biochemical tests should be done to make dx
What is early treatment of temporal arteritis?
What are the main cerebral arteries?
What are the anatomical locations of intracranial aneurysms?
Most subarachnoid hemorrhage are caused by ruptured intracranial saccular (berry) aneurysm
Anatomical location of intracranial aneurysm
* Anterior circulation (85%)
o Bifurcation of MCA
o Junction of ACA and anterior communicating artery
o Junction of ICA and posterior communicating artery
* Posterior circulation (15%)
o Top of basilar artery
o Junction of basilar artery and superior cerebellar artery
o Junction of basilar artery and anterior inferior cerebellar artery
o Junction of vertebral artery and posterior inferior cerebellar artery
What are the RF for cerebral aneurysms?
What is the different types of aneurysm?
Saccular (berry) aneurysm: Thin-walled protrusion from intracranial arteries that composed of a very thin or absent tunica media and a severely fragmented or absent internal elastic lamina
Fusiform aneurysm: Enlargement or dilatation of entire circumference of the involved vessel that may in part be formed due to atherosclerosis
Mycotic aneurysm: Result from infected emboli due to infective endocarditis
What is the clinical manifestation of cerebral aneurysm (unruptured and ruptured)?
What are imagings for cerebral aneurysm?
General features
* Most intracranial aneurysms are incidental findings
Imaging modalities
* CT angiography
* MRI angiography
* Cerebral angiography
What are the indications for intervention of cerebral aneruysm?
What surgical treatment options are there?
What subtypes of congenital vascular malformations of CNS are there?
- AVM: possible neurological sequelae (most dangerous)
- Cavernous malformation (cavernous angioma): possible neurological sequlae
- Developmental venous anomalies (venous angioma); more benign
- Capillary telangiectasia: more ebenign
Describe the different cerebral vascular malformations
What is clinical manifestation of AVM?
What are the imaging Ix for cerebral vascualr malformatino?
What is the grading scale for intracranial AVMs?
What surgical treatment options are there?
What is classification of stroke?
Define transient ischemic attack?
What is the scoring system for assessing whether patient should be admitted into hospital?
What are the causes of ischemic stroke (thrombosis) –> large vessel (intracranial, extracranial, small vessel intracranial)?
What are the ischemic stroke causes (embolism) cardiac and aortic source?
What are the ischemic stroke causes systemic hypoperfusion?
What are the ischemic stroke causes (hypercoagulability)?
What are the causes of hemorrhagic stroke?
What is pathological appearance of stroke?
Pale infarction which is swollen and slightly softened
* Blood cannot reach the area distal to obstruction and thus pale in appearance
Hemorrhagic infarction
* Reperfusion to ischemic part of the brain will lead to hemorrhagic appearance
o Capillaries are damage during ischemia and can no longer stand the BP when blood flow is reestablished
Cracking and liquefactive necrosis
Resorption with replacement by fluid filled cavities
What is the histological appearance of stroke?
What are cortical signs indicative of cortical stroke (ischemic)?
What are subcortical signs indicating location of ischemic stroke?