Previous Questions Flashcards
Describe the ‘mental status examination’.
General behaviour and appearance:
- Is the patient normal, hyperactive, agitated, quiet?
- gestures, involuntary movements, twitches, immobile
- Is the patient neat or slovenly?
- Does the patients attire match their age/sex/background? are they well groomed?
Stream of talk:
- volume, rate, coherence
- does the patient converse normally? is the speech rapid, incessant, under great pressure, or is it slow and lacking in spontaneity?
- is the patient discursive and unable to reach conversational goal?
Mood and affective responses
- is the patient euphoric, agitated, inappropriately gay, giggling, or silent, weepy, angry?
does their mood swing in an appropriate way relative to the conversation?
- normal mood = euthymia, elevated = euphoria, dampened = dysphoria
Content of thought:
- does the patient have illusions, delusions, or hallucinations?
- Are they preoccupied with fears of cancer or dying?
- normal/odd thoughts, word usage, continuity
Intellectual capacity:
- is the patient bright, average, dull, or obviously demented or mentally retarded?
Sensorium:
- Consciousness, attention span, orientation of time and place, memory (recent/remote), fund of information (recent events etc.) insight, judgement, and planning, calculation
Consciousness:
- awareness of self and environment
- orientation of self, place, time and situation
e. g. of altered consciousness in disorientation and delirium
Level of consciousness/coma:
- Glasgow coma scale (GCS) → Eye opening, best verbal response, best motor response to verbal or painful stimuli (1 being worst, 6 being best scores)
Higher cerebral function:
Cognition – Communication: Aphasia, Alexia, Agraphia, Acalculia, Agnosia, Apraxia
Memory – Immediate recall, short/long term memory
Reasoning & problem solving
Emotional state E.g. depression, anxiety, apathy, elation
List the questions and explain the diagnostic catechism
The diagnostic catechism is a sequence of events which assist in directing the neurological examination based on the presenting signs and symptoms (if any) which will help with the arrival of a provisional and differential diagnoses. This is via use of:
- Neuroanatomical knowledge
- Neurological disease knowledge
- Neurological examination
- Does the patient have a lesion?
- is the patient suffering from an emotional disorder, organic disorder, or both? (emotional or functional can manifest into physical sac although there is no physical basis)
- CAN NOT RELY ON SYMPTOMS ONLY MUST HAVE A SIGN
- the appropriate near physical exam will help is discover any signs, so need to have good clinical skills. Find a sign - it will have distinguish between functional and organic conditions!
NB: Some conditions only have signs during ictal periods E.g. hypoglycemia, some epilepsies etc. & some psychiatric conditions can mimic organic conditions: Catatonia in psych conditions mimicking diffuse encephalopathy or status epilepticus (pt stares appears conscious but is unresponsive)
- If so where is the lesion?
- How will the presence of a sign help us to arrive at a diagnosis?
- It may allow us to determine which organ/ organs or system/systems are implicated.
- Try to figure out what part of the body must be affected in order for the pathology to occur. Also try to figure out if the lesion is structural or biochemical
Using the sign found, we can decide which organ(s), or system(s) the lesion is affecting & what exam is appropriate
CNS Vs PNS
Structural Vs biochemical
Focal, multi-focal, diffuse, generalized
E.g. Weakness:
- UMN type → UMN exam, affects functional groups of muscles
- LMN type → LMN exam, affects individual muscles or muscles supplied by an individual nerve
- NMJ type → NCS etc, weakness of small striated muscles during exertion e.g. eyelid in MG
- Muscle origin → EMG, biopsy etc
- Arterial supply etc → vascular exam
- Electrolytes → blood tests
- Hypoglycaemia → blood glucose levels
E.g. Abnormal movement: Which part of the body would have to be affected for this abnormal movement to occur?
- Resting tremor → BG (substantia nigra)
- Chorea → BG (sub-thalamic nucleus)
- Intention tremor → Cerebellar
- Fasiculation → Atrophied skeletal muscle
- Etc.
- What is the lesion or the simplest provisional diagnosis?
- How do we arrive at a dx now that we have a list of ssx and have thought about where the lesion lies anatomically?
- Need to know our pathology and manifestations of diseases . We can then attempt toes if any disease can account for most or all of the clinical manifestations. Usually arrive at several ddx
Collate the SSx to determine which neurological disease(s) best fit the clinical picture and Hx Consider Pt: - Age - Gender - Race - Risk factors
E.g. Raised ICP:
- Granuloma
- Leukemia
- CNS neoplasm (primary or metastatic)
- Aneurysm
- what clinical or laboratory tests will confirm or reject the provisional diagnosis and establish the final dx?
- Must take into account: Can the test provide evidence to support or reject the provisional dx?
- Is the test the simplest, cheapest and safest one?
- When faced with a hopeless or untreatable disorder, have you taken all reasonable steps to exclude a treatable disorder? - what is the optimum management?
- State the realistic therapeutic goals - consider relevant emotional or socioeconomic issues.
- What other services might help the patient? e.g. OT, physic etc.
- Are other persons at risk (contagious or hereditary disorders?
- Follow up of the patient
Example: Pt F# hip 6 months ago complains of unsteadiness:
- Is this Symptom organic or emotional (fear of falling over)
- We cannot answer this until we find a sign
- If -ve cerebellar, sensory and motor exams → more likely to be emotional
- If +ve cerebellar, sensory exams bilaterally in feet → more likely to be organic pathology (SIGNS FOUND) → What pathology is common, and affects bilaterally at the distal legs → Diabetic polyneuropathy
Why do we use qualifiers? Give an example…
Qualifiers are descriptors used when marking down presenting ssx. They are used to give the best possible information regarding the presenting ssx, as well as aid the diagnostic process (figure out the ddx).
- Where must this lesion be to create the ssx (CNS Vs PNS) → organize it in order from highest (cortical) to lowest (intrinsic muscle) E.g. Psychogenic → Cerebrum → BG → Cerebellum → Brainstem → UMN → LMN → NMJ → Intrinsic muscle
- Use descriptive terms for each manifestation E.g. unilateral, symmetrical, proximal, diffuse, constant, gradual, resting, severe, early onset, familial ETC. (think of opposites to all those listed)
Help the ruling in or ruling out certain pathologies & the site of the lesion based on their usual presentations
e.g. muscle atrophy
unilateral –> peripheral nerve, spinal nerve
bilateral –> myopathy, metabolic, hereditary
symmetrical –> myopathy, metabolic, hereditary
asymmetrical –> vascular
proximal –> myopathy
distal –> peripheral neuropathy
diffuse –> peripheral neuropathy
localised –> peripheral nerve, mm injury
What are some LMN ssx give an example.
- rapid atrophy (early localised)
- fasciculations
- single mm weakness (myotomal)
- early localised unilateral hyporeflexia/areflexia (decrease DTR)
- localised unilateral flaccid paralysis
What are ssx in myopathy and give a qualifier (can’t use the same ssx as above)
- symmetrical proximal mm weakness
- bilateral proximal mm group atrophy
- high incidence of family hx or similar disorder
- low amplitude EMG waves
- mm contractures causing reduced ROM
Define cerebral angiography
- deviations
- indications
- contraindications
- complications
Cerebral angiography – Visualization of the cerebral blood vessels and blood flow via the use of catheter introduced contrast medium (iodine) and X-ray scanning to identify lesions of the cerebral vasculature or tissues
Deviations from normal:
- Vascular tumours containing multiple AV fistulas
- Non-vascular tumours (compress vasculature E.g. absceses or hematoma)
- AV malformations (increased blood and therefore pressure in veins)
- Narrowing and obstruction of the vascular lumen E.g. atheroma
Indications:
- Suspected intracranial trauma E.g. hemorrhage
- Suspected intracranial vessel occlusion E.g. atheroma or vascular tumour
- Suspected intracranial mass E.g. tumour, hematoma, abcesses (distort surrounding vessels)
- Investigate raised ICP
- AV malformations (abnormal bloodflow between arteries and veins = Increased pressure in area)
- Narrowing and obstruction of vascular lumen E.g. berry aneurysms or Charcot-Bouchard micro aneurysms or stenosis of arteries such as IC
Contraindications:
- Pregnancy
- Breastfeeding (delayed by 24 hours after contrast medium injection)
- Severe renal disease (cannot expel iodine)
- Non-compliant patient E.g. cannot sit still
Complications (Rate very low)
- Allergic reaction to contrast medium
- Renal failure due to contrast medium
- Arterial rupture & hemorrhage
- Thrombus & embolus formation
- Stroke (catheter dislodges plaque)
- Infection
- Bleeding
- Cancer (radiation)
- Iatrogenic spread of disease
Define PET scan and discuss
- normal
- deviations
- indications
- contraindications
- complications
PET = Positron Emission Tomography:
- Computer based imaging technique which provides a picture of the brains metabolic and physiologic tissue function, rather than structures (CT, MRI)
- Substances E.g. glucose, dopamine transporters that’re labelled with a radioactive tracer are tracked
- Provides quantitative information about brain function, in which measurements of marked substances such as glucose correlate to blood flow, and therefore brain activity. I.e. More brain activity = more blood flow w/substance (RADIONUCLEOTIDE DOES NOT ENTER TISSUE)
- Provides complementary functional information to anatomic imaging such as MRI
- One of the most effective diagnostic tools in detecting whether a cancer remains after surgery. However, very little machines in Aus & price Is very high (not accessible). PET is becoming more widely used as the cost and availability improves
Normal values:
- Particular part of brain becomes more active & blood flow is increased E.g. temporal lobe when listening, occipital lobe when looking, frontal lobe when thinking. I.e. NORMAL cerebral activity
Deviations:
- Areas of no/low brain activity and therefore blood E.g. Parkinson’s causing reduced bloodflow to the subtantia nigra
- Areas of overactivity E.g. Epilepsy
- Huntington’s
- Myocardial infarction
- CVA
- Epilepsy
- Dementia
- Tumours etc
- Pulmonary oedema etc
Indications:
- Determinations of regional metabolism in the heart and brain
- Studies tissue permeability
- Measurement of sizes of infarcts
- Investigate tissue physiology in psychosis
- Assessment of effects of cancer treatment by assessing malignant tissue & normal tissues
Contraindications:
- Pregnancy
4 findings of a SPECT scan
SPECT = Single Positron Emission Computed tomography (Same thing to PET, just cheaper and poorer resolution, also uses different nucleotides)
SPECT also used in complementing anatomical MRI with function
SPECT inferior to PET due to poorer resolution and sensitivity (PET results in 2 photons = better quality)
Deviations from normal: (as above → Increased or decreased uptake)
Indications:
- Localization of epileptigenic foci
- Cerebrovascular disease (e.g. infarct, ischemia)
- Brain tumours
- Head trauma
- Assessment of radiation injury
- Infectious diseases
Contraindications:
- Pregnancy
Complications:
- Radiation exposure
4 findings of a SPECT scan:
- Increased perfusion/uptake
- Decreased perfusion/uptake
- Location of epileptogenic foci
- Location of a tumour
In CSF examination list the conditions in which you would see
- High protein – bacterial meningitis
- Blood presence – cerebral haemorrhage
- Neutrophil presence – bacterial meningitis
- Inc pressure – tumour, haemorrhage, oedema, haematoma
What is somatosensory evoked potentials? Give four findings and what they may indicate.
SSEP examines the pathways form the nerves of the limbs to the brain. The SSEP test can help to study the function of these nerves, the spinal cord and brain SSEPs record the somatosensory electrical potentials travelling through the peripheral nerves toward the CNS (ALS, DCML, spinocerebellar)
Process:
1) Stimulate limb
2) Potentials recorded in the peripheral nerve, spinal cord and brain
3) Interpretation of SSEP trace
Possible findings:
- Slowing of conduction velocity E.g. possible demyelination or NT disorder i.e. MS or MND
- Reduced amplitude e.g. partial neuropathy
- Absence of response e.g. neuropathy
- Where the pathway pathology lies E.g. peripheral nerve conduction fine, stops in spinal cord
Clinical manifestations of a cluster HA
- Episodic or chronic
- Age of onset usually 20-40
- Males 3-4x higher than women
- Autosomal dominant in 5% cases
- Pathophys and aetiology not well known → Acute attacks involve activation of posterior hypothalamic grey matter which results in central sensitization of trigeminal nociceptive pathways which results in blood vessel dilation which compresses the trigeminal nerve
- Vascular dilation secondary to primary neuronal discharge
During cluster-period, attacks occur regularly and may be provoked by:
- Alcohol (vasodilation)
- Histamine (vasodilation)
- Nitroglycerine (Drug therapy for angina, vasodilation)
Clinical course:
- Attacks occur in series (cluster periods) lasting weeks or months separated by remission lasting months or years (episodic)
- Clusters occur more than once a year without remission, or remission period is less than a month (Chronic)
- 10-15% have chronic symptoms without remission (suicide HA)
Ssx:
- Rapid onset, severe knife life UNILATERAL pain (strictly unilateral)
- Pain is orbital, supraorbital, temporal (also combination of these sites)
- Pain lasts 15 minutes to 3 hours
- Pain occurs once every other day to 8 times a day
- Pt are restless or agitated during attack, pain can be excruciating hence patients are unable to lie down (increased ICP) and characteristically pace the floor
- HA disappears as abruptly as it appeared
Also, Ipsilateral autonomic findings:
Eye - conjunctival injection (red eye), lacrimation, miosis, ptosis & eyelid edema (HORNER’s)
Sinuses - nasal congestion & rhinorrhea, forehead and facial swelling & flushing/sweating
Diagnostic criteria (At least 5 attacks fulfilling criteria):
- Severe or very severe unilateral pain
- Orbital, supraorbital or temporal pain lasting 15 minutes to 3 hours if untreated
- Attacks have frequency of one every other day to 8 a day
- HA is accompanied by at least one autonomic finding or a sense of restlessness or agitation
Clinical manifestations of migraine with out aura
Terminology – Previously called Common migraine
- Commonest migraine subtype (higher average attack frequency)
- Usually more disabling then a migraine WITH aura
- Often has a clear relationship with the menstrual cycle
- Once regarded as primarily vascular, however now considered neurobiological disorder (as for TTH) → Originates in CNS tissue rather than vessels (no changes to cerebral blood flow during episode suggests NO Cortical spreading depression)
Classification
- Pure menstrual migraine without aura
- Menstrually-related migraine without aura
- Non-menstrual migraine without aura
Typical clinical features
- Recurrent attacks lasting 4-72 hours
- Unilateral location
- Pulsating quality (Cluster is stab-like, TTH is non-pulsatile & band like)
- Moderate to severe intensity
- AGG by physical activity
Often associated with:
- Nausea
- Malaise
- Photophobia
- Phonophobia
Diagnostic criteria
At least 5 attacks following criteria:
- HA lasts 4-72 hours (untreated or unsuccessfully treated)
- HA has at least 2 of the following → Unilateral, pulsating, moderate/severe pain
- HA AGG or causing avoidance of routine physical activity such as walking
- HA accompanied by at least one of → photophobia, phonophobia (not due to other condition)
Clinical manifestations of tension HA
Classification of TTH
- Episodic
- Chronic
- Probable
Episodic (two types):
- Infrequent (HA episode less than once a month)
- Frequent (1-4 episodes/12, considerable disability & associated analgesic & prophylactic medication use)
Chronic – More than 15 episodes/12 causing greatly decreased quality of life, high disability and tangible costs
Epidemiology
- Most common type of primary HA (90% of all HA)
- Lifetime prevalence in the general population ranges in different studies (30-78%)
Aetiology
- Least studied primary HA disorder out there, despite it has the highest socio-economic impact
- Previously considered to be psychogenic → newer studies suggest a neurobiological basis for the more severe subtypes of TTH I.e. CNS tissue casuing HA (Chronic TTH)
- Peripheral pain mechanisms are most likely to play a role in BOTH types of episodic HA
- Central pain mechanisms are thought to play a role in Chronic TTH
Clinical features
Episodic I.e. stress HA:
- Usually triggered by stress/anxiety/anger/fatigue
- Short duration of episode
Chronic:
- Can result from anxiety or depression (chronic episodic)
- Daily/continuous HA (always present)
- Pain intensity varies during a 24-hour cycle
Pain is:
- Steady
- Non pulsatile
- Moderate intensity
- Unilateral OR bilateral (Cluster is severe pain, strictly unilateral)
- Aching
- Vice/band like
- Usually begins occipitally → can involve frontal & temporal areas (Cluster HA is orbital, supraorbital & temporal)
- Recurrent (often afternoons/evenings)
Typical clinical features: - Tenderness of peri-cranial muscles → Post. Cx, temporalis & masseters (upper-X teeth clenchers) - Dizziness - Blurred vision - Tinnitus Other: - Insomnia - Fatigue - Irritability - Poor appetite - Difficulty concentrating
Typical Pt
- Tense, anxious female
- Work posture requiring sustained contraction of post. Cx E.g. desk worker
- Clenches teeth (anxiety)
Dx & Ddx
- Diagnosis usually made via history and clinical exam
- TTH SSx are confused confused with migraine W/o aura
List 5 HA red flags and why they are considered Red Flags
1) HA in a person older than 40-50 years of age (cancers, stroke etc. higher incidence in older pop)
2) Sudden onset of intense pain “worst HA of my life” (new pathology, stroke etc)
3) Marked change in HA pattern, such as increased frequency, intensity or duration (progression of a pathology, e.g. metastasis, growth)
4) HA starting post head injury
5) HA worsening with exercise, sex, coughing or sneezing (raised ICP)
6) HA’s always occurring on the same side of the head (Lesion on one side)
7) HA that wake a person
8) Persistent or unexplained vomiting
9) New onset HA in a person with certain medical conditions E.g. HT, cancer or AIDS
10) HA with sign of systemic illness E.g. fever, stiff neck, rash
11) HA with associated neurological ssx:
- Diploplia
- Blindness
- Abnormal eye movements
- Sensory loss
- Sudden lack of balance, falling & dizziness
- Confusion
- Inappropriate behavior
- Seizures
- Aphasia
- Ataxia
- Weakness in arm or legs
- Syncope
Medication Overuse HA (rebound HA)
Definition:
Is a type of HA that occurs in people who regularly overuse analgesics for their TTH or migraine
i.e. when the analgesic is not taken the patient experiences an analgesic withdrawal HA
Epidemiology:
- affects 1-2% of the general population in EU, North America and Asia
- being 3-5 times more common in women
- found to be 3rd most common cause of HA
Pathogenesis:
- Following a period of unusually severe or frequent TTH or migraines, analgesics are taken more often than usual
- In time the body becomes accustomed to the pain killers
- A withdrawal HA then develops if analgesics are not taken within a day or so of the last dose
- sufferers assume its just another TTH/migraine and take another dose of the painkillers
- As the analgesia wears off a further withdrawal HA develops and vicious cycle ensues resulting in a chronic daily HA (therefore in time sufferers have HA on most/every day and take analgesics each time
BUT MOH does not develop when painkillers are taken for other conditions i.e. arthritis
Clinical features: Pain: - oppressive - in the am, with exercise and stress Other: - nausea - irritability - depression - insomnia
Meds involved: codine paracetamol NSAIDS migraine meds
