Mock Exam (DT) Flashcards

1
Q

List and discuss 4 components of the mental status examination. (8 marks)

List and discuss components of the mental status examination. (10 marks)

A

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

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2
Q

4 LMN manifestations with descriptors. (8 marks)

A

Myotomal weakness
Early, localized and unilateral Atrophy & fasciculation
Early, localized and unilateral reduced DTR
Localized unilateral flaccid paralysis

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3
Q

4 manifestations of myopathy with descriptions (8 marks)

A

Bilateral proximal muscle group fatigue & weakness (cardinal finding)
Bilateral proximal muscle group atrophy (late finding)
Muscle contractures causing reduced ROM
Diffuse Hyporeflexia (late finding)
Chronic familial weakness

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4
Q

Diagnostic catechism (8 marks)

List and describe questions of the diagnostic catechism. (10 Marks)

A

..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
  1. 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)

  1. 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
    3. 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
  1. 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?
  2. 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

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5
Q

List clinical manifestations of a cluster headache. (5 marks)

A
Episodic or chronic
Age of onset usually 20-40
Males 3-4x higher than women
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
Runny nose
Red Eye
Congested sinuses
Flushing/sweating
Lacrimation
Miosis
Ptosis
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6
Q

List clinical manifestations of medication overuse headache. (5 marks)

A

..

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7
Q

Why use descriptors for SSx- provide examples. (6 marks)

A

Choose a manifestation (motor or sensory)

  • Where must this lesion be to create the ssx (CNS Vs PNS) à organize it in order from highest (cortical) to lowest (intrinsic muscle) E.g. Psychogenic à Cerebrum à BG à Cerebellum à Brainstem à UMN à LMN à NMJ à 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)
  • Descriptors assist in narrowing the potential Dx, with regard to ruling in or ruling out certain pathologies & the site of the lesion based on their usual presentations
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8
Q

Anti-acetylcholine receptor antibody test.

A

Approximately 85-90% of patiets with MG express three types of auto immune bodies ro the acetylcholine receptor (AChR):
Binding
Blocking
Modulating
Deviations from normal values
An absense of pathological antibodies
Serum auto-ab’s are found in 80-90% of patients with generalised MG
Serum auto-antibodies found in 55-70% of patients with ocular MG
auto-Ab’s titrates tend to be higher in female
Indications
To assist in the:
evaluation of muscle weakness
diagnosis of MG in patients with:
− Drooping eyelid; Double vision; Decreased eye movement control.
− Dysphagia with choking, drooling and gagging.
− Slurred speech.
− Weak neck muscles; trouble holding up head.
− Difficulty breathing.
− Difficulty walking; altered gait.
− Specific muscle weakness but normal feelings/sensations.
− Muscle weakness that worsens with sustained effort & improves with rest.
evaluation of MG disease activity
evaluation of response to therapy

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9
Q

Define cerebral angiography (normal values, indications and contraindications) (6 marks)

A

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
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10
Q

List four neurological pathologies that would warrant a lumbar puncture.

List two contraindications of a lx puncture. (6 marks)

A
  • Spinal cord neoplasm
  • Cerebral hemorrhage
  • Meningitis
  • Encephalitis
  • Degenerative brain disease
  • Raised ICP - tonsillar herniations
  • Spinal joint degeneration
  • Uncooperative patient
  • Infections near puncture site
  • Psychosomatic illness
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11
Q

Define EEG (2 marks)

Define EMG

A

EEG
What is it?
- Records the electrical activity of the brain with sensitive electronic equipment from recording electrodes that are placed at measured intervals on the persons scalp
- Active neurons generate electrical activity in the form of Aps
- EEG’s provide important information on:
- Background electrical activity
- Epileptiform discharges

Deviations from normal
Seizures 
CNS lesions 
Syncope 
Panic attacks 
Parasomnias (night terrors)
Hypnic jerks or sleep starts 
Deviation eg. Epilepsy

Indications
To investigate epileptic states
To diagnose cerebral lesions
To determine cerebral death in comatose patients
To monitor cerebral blood flow during surgery
Note:
as of 2013 EEG are not recommended for the diagnosis of headache disorders
Rationale:
- Clinical features have better diagnostic accuracy for primary headaches
- Neuroimaging has higher sensitivity than EEG to evaluate for a mass lesion, if clinically suspected

EMG
What is it?
- An audio or visual record of the electrical activity of a skeletal muscle
- Produced via a stimulation electrode that is either inserted into the muscle or placed on the skin over the muscle
2 types:
Skin pad and intramuscular

Indications

  • Aids in the diagnosis of neuromuscular disorders
  • Muscle spasticity
  • Nerve impingement i.e. back, neck etc
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12
Q

List 2 indications of a lx puncture.

A

Lumbar puncture
PRESSURE:
Abnormal values:
Tumour, haemorrhage, haematoma, oedema, scarring, foreign body, or intervertebral disc.
COLOUR
Abnormal values
Blood from subarachnoid bleeding or from the lumbar needle penetrating a blood vessel.
BLOOD
Abnormal values
Blood in the CSF indicates cerebral haemorrhage into the subarachnoid space or a traumatic tap.
CELLS
Abnormal values
The presence of polymorphonuclear leucocytes (neutrophils) in the cerebrospinal fluid indicates bacterial meningitis or cerebral abscess. The presence of mononuclear leucocytes indicates viral or tubercular meningitis or encephalitis.
CULTURE AND SENSITIVITY .
Abnormal values
Cultured organisms may include atypical bacterial, fungi, or
Bacterium tuberculosis.

Deviations from normal
PROTEIN
Infectious or inflammatory processes such as meningitis, encephalitis, or myelitis.
Tumours may also cause an increase in protein count. Patients with multiple sclerosis, neurosyphilis, or degenerative cord or brain disease will have an elevation of the globulin fraction of total protein.
GLUCOSE
- A CSF glucose level of less than 40% of the blood glucose level may indicate meningitis or neoplasm.

Indications
CHLORIDE
The Cl- concentration in the CSF may be decreased in patients with meningeal infections, tubercular meningitis, and conditions of low blood chloride levels.
LACTIC DE- HYDROGENASE
Elevated LDH levels indicate infection or inflammation (eg., bacterial meningitis).
CYTOLOGY
The presence of tumour cells indicates neoplasm.
SEROLOGY FOR SYPHILIS
Positive results on Wassermann, Venereal Disease Research Laboratory (VDRL), or fluorescent treponemal

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13
Q

List 2 indications of myelography

A

An imaging procedure in which a needle is inserted into the spinal canal, & contrast material injected into the space around the spinal cord & nerve roots (subarachnoid space)
Myelography still remains the diagnostic procedure of choice in:
patients with a pacemaker
patients with old fusions
claustrophobic patients
identification of spinal CSF leaks
MRI/CT has failed to provide adequate information

Deviations from normal
IV disc herniation/ruptures: myelograms can accurately locate the disk(s) involved, & demonstrate spinal nerve impingent
To determine if osteophytes are causing spinal /nerve root impingement
To determine if osteophytes are causing spinal stenosis
For the accurate location of tumours
To identify a range of other conditions:
e.g. infection, meningitis, vasular abnormalities, traumatic injuries etc

Indications
Myelography is most commonly used to detect suspected abnormalities affecting the:
spinal cord
spinal canal
spinal nerve roots
blood vessels that supply the spinal cord
Myelography is also used to:
- To visualise the extent of a known lesion
- To investigate persistent, unexplained pain, numbness, or weakness
- To determine if an IVD herniation is compressing nerve roots, spinal cord or cauda equina
- To detect suspected spinal stenosis caused by osteophytes or thickening of adjacent ligaments

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14
Q

List 2 indications of EP

A
  • MS
  • Neurological disorders
  • Spinal cord injury
  • Parkinsons
  • Auditory Disorders
  • Areas of brain dysfunction post trauma
  • Pinpoint tumors

Types of EP

  • Somatosensory (SSEP)
  • Brain Auditory (BAEP)
  • Visual (VER)
  • Motor (MEP)
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15
Q

What are 4 indications that warrant a nerve conduction test. (4 marks)

A

What is it?

  • Nerve conduction velocity is a technique used to study nerve or muscle disorders
  • It measures the speed at which motor nerves transmit signals
  • Two types → motor and sensory

Types
Motor nerve conductions velocity test (MNCV)
- Evaluated by recording the compound muscle AP (CMAP) that is created when a muscle contracts following the electrical stimulation of motor nerve fibres supplying that muscle
- The CMAP is the sum of all the APs occurring individually in the contracting muscle fibres
Sensory nerve conduction velocity test (SNCV)
- Determined by examining the sensory nerve AP (SNAP) that is obtained from the nerve itself, by recording electrodes on the skin, following electrical stimulation of the nerve being investigated
- The SNAP is the sum of all the APs generated in the sensory nerve fibres y the stimulatory electrical shock
Indications
Radiculopathy (one of the most common reasons for having and NCV ordered)
Suspected nerve disorders
- MND
- Entrapment neuropathies
- Carpal tunnel syndrome
- Polyneuropathies
- Peroneal neuropathies
- Plexopathies (brachial/lumbar)
Neuromuscular disorders
- Myasthenia gravid
- Lambert Eaton syndrome
- Botulism
Some myopathies

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16
Q

SPECT

A
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 à 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
17
Q

PET

A

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
18
Q

Clinical manifestations of a migraine without Aura. (4 marks)

A

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) à 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 à Unilateral, pulsating, moderate/severe pain
- HA AGG or causing avoidance of routine physical activity such as walking
- HA accompanied by at least one of à photophobia, phonophobia (not due to other condition)

19
Q

Clinical manifestations of a Cluster HA

A

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 à 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
20
Q

Clinical manifestations of a Tension HA

A

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 à 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 à can involve frontal & temporal areas (Cluster HA is orbital, supraorbital & temporal)
- Recurrent (often afternoons/evenings)
Typical clinical features:
- Tenderness of peri-cranial muscles à 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

21
Q

Clinical manifestations of a Migraine

A

Migraine HAs are consider to be the world’s most common serious neurological disorder, considered to be one of the top 10 most debilitating conditions

Migraine with aura ‘Classic migraine’
Aetiology unknown
The manifestation seen in migraine with aura are thought to be related to Cortical spreading depression (CSD)
CSD often originates in the visual or somatosensory cortex, hence the aura is commonly experiences or as a tactile tingling

Clinical features
Recurrent disorder
Attacks of reversible focal neurological symptoms
Usually develop gradually over 5-20 mins
Last <60 mins
Exhaustion following the HA
Focal neuro ssx
Visual (usually) e.g. photophobia
Unilateral paraesthesia (hand, periorally)
Aphasia
Hemiparesis
Hemisensory defects
Less commonly the HA can be absent
Diagnostic criteria
At least 2 attacks fulfilling the following criteria:
– Presence of an aura
– Not attributable to another disorder (e.g. stroke, MS etc)

22
Q

Clinical manifestations of a Cranial arteritis

A

An idiopathic vasculitis which usually restricted to the cranial vessels
Is an important cause of HA in the elderly
Typical patient >60 years old

Clinical features 
Unilateral or bilateral
Temporal, fronto-occipital or occipital
Pain in jaw
Palpable nodules on superficial temporal arteries
Variable intensity
Complication 
Blindness due to retinal artery occlusion
23
Q

Clinical manifestations of a Nasal/sinus HA

A
The most common cause is acute inflammation of the paranasal sinuses 
Clinical features						
• Pain (over the affected sinus)
• Fever
• Swelling (over the affected sinus) 
• Tenderness (over affected sinus) 
• Engorgement (of nasal structures) 
Diagnosis 
Clinical examination
Sinus x-ray 
Often misdiagnosed as vascular HA/TTH
24
Q

Clinical manifestations of a Trigeminal neuralgia

A

Trigem neuralgia:

  • Compression via tortuous arteries in the posterior fossa E.g. Trigem ganglion tumour, MS, brainstem infarct
  • Hx – Brief episodes of lightning-like stabbing pain felt when touching areas such as lips during eating, talking etc with exacerbations in spring & autumn
  • SSX – Pain in clusters, refractory period where pain is fleeting, occurs in one branch of trigem (opthal, max, mandib)

Cranial Neuralgia:

  • Pain in head from trigeminal nerve, glossopharyngeal, vagus, upper Cx roots & nervus intermedius (Facial nerve)
  • Stimulation of these nerves via compression, distortion, exposure to cold, irritation, lesions etc. give rise to stabbing or constant pain felt in the area innervated by the nerve
  • Causes à Herpes zoster, structural abnormality, idiopathic
25
Clinical manifestations of a MOH
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 ```
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CSF study- What is CSF, what are indications of CSF. What could cause a change to; pressure, blood, protein, neutrophils? (10 marks)
on google doc