Neurological Conditions Flashcards
1
Q
What is a stroke
A
A cerebrovascular event that is caused by abnormal perfusion of cerebral tissue.
A common medical emergency that requires urgent recognition and treatment.
A clinical syndrome characterised by sudden onset of rapidly developing focal or global neurological disturbance, which lasts more than 24 hours or leads to death.
2
Q
What are the two types of stroke
A
Haemorrhagic
Ischaemic
3
Q
What is an ischaemic stroke
A
Are due to occlusion of blood vessels that supply the brain parenchyma leading to infarction (tissue necrosis secondary to ischaemia).
4
Q
What is a haemorrhagic stroke
A
Haemorrhagic strokes are the result of bleeding within the brain parenchyma, ventricular system or subarachnoid space.
5
Q
What is the Bamford/Oxford classification
A
Used to sub classify ischaemic strokes
It differentiates ischaemic strokes based on the presenting features which correlated with the cerebral territory affected
Total anterior circulation stroke (TACS)
Partial anterior circulation stroke (PACS)
Lacunar stroke (LACS)
Posterior circulation stroke (POCS)
6
Q
How common are strokes
A
~110,000 per year in England
Mortality from first ever stroke is 11%
7
Q
What is the cause of ischaemic strokes
A
- Caused by occlusion of cerebral blood vessels
- Most common accounting for 85% of cases
- Can result from a thrombus within a vessel, embolus arising from a distant site, or rarely, a dissection.
8
Q
What is the cause of hemorrhagic strokes
A
- Result from bleeding
- Accounts for 15% of cases
- Most commonly due to hypertension
- Other causes include vascular malformations, brain tumour, vasculitis, bleeding disorders
- Trauma is another major cause but usually classified as part of traumatic brain injuries
9
Q
What are the risk factors for strokes
A
Smoking Diabetes mellitus Hypertension Hypercholesterolaemia Obesity AF Carotid artery disease Age Thrombophilic disorders Sickle cell disease
10
Q
How do each type of stroke present
A
A stroke presents with sudden, focal neurological deficit that reflects the area of brain devoid of blood flow.
Haemorrhagic:
- More likely to present with global featurese
- Headache
- Altered mental state
- Nausea/vomiting
- Hypertension
- Seizures
- Focal neurological deficits
Anterior ischaemic stroke:
- TACS, PACS, LACS
- Develop a constellation of features dependent on the extent and location of the infarct
- Unilateral weakness and/or sensory deficit to face, arms or legs
- Homonymous hemianopia
- Higher cerebral dysfunction: dysphasia, visuospatial dysfunction
- Classically, isolated infarction of the anterior cerebral artery leads to contralateral leg wekness only
Posterior ischaemic stroke:
- Posterior circulation is composed of the vertebrobasilar artery system
- This supplies the brainstem, cerebellum and occipital cortex
- Therefore, posterior strokes can affect balance, vision and cranial nerves
- Dizziness
- Diplopia
- Dysarthria and dysphagia
- Ataxia
- Visual field defects
- brainstem syndromes
11
Q
What are the differentials for stroke
A
Numerous conditions present similarly to stroke - aka ‘stroke mimics’
Toxic/metabolic:
- hypoglycaemia
- drug/alcohol consumption
Neurological:
- seizure
- migraine
- Bell’s palsy
Space occupying lesion:
- tumour
- haematoma
Infection:
- meningitis/ encephalitis
- systemic infection with ‘decompensation’ of old stroke
Syncope:
- extremely uncommon presentation of TIA
- consider causes of syncope
Non-organic:
-functional neurological disorders (FND)
12
Q
How is a suspected stroke investigated
A
Any patient with suspected stroke, refer to stroke unit urgently
Initally clinically diagnosed based on history and examination
Fast test used in community to screen patients for urgent transfer
In hospital, NIHSS score is used in correlation with urgent cross-sectional imaging (CT head ± CT angiography)
Clinical assessment:
- Onset and duration of symptoms
- Associated symptoms
- Neurological deficit
- Cardiovascular risk factors
- Co-morbidities
- Anticoagulation history
- Contraindications to thrombolysis or thrombectomy
FAST test (Face Arm Speach Time)
- Positive test if:
- New facial weakness
- New arm weakness
- New speech difficulty
CT head is the key investigation in patients presenting with a suspected stroke
Bedside:
- Observations
- Blood glucose
- ECG (AF)
Bloods:
- FBC
- UandEs
- Bone profile
- LFT
- ESR
- Coagulation
- Lipid profile
- HbA1c
Imaging:
- CT head
- CT angiography
- MRI head
Special tests:
- Echocardiography
- Carotid dopplers
- 24 hour tape
- Young stroke screen
13
Q
What are important discussions to have with a stroke patient
A
Advise not to drive and to inform the DVLA
14
Q
How is each type of stroke treated
A
“Acute management:
Determine type of stroke on the initial CT
Haemorrhagic stroke:
Management depends on the extent of the bleed and suitability for neurosurgical interventions
In small bleeds, no need for surgery
Surgical intervention may be required for larger bleeds with significant neurological deterioration
Includes use of decompressive hemicraniectomy or suboccipital craniotomy for posterior fossa bleeds
Ischaemic stroke:
If the CT head does not reveal any signs of intracerebral bleeding then the patient is managed as an ishcemic stroke
A initial decision is made about suitability of thrombolysis based on stroke severity, contraindications and timeframe
Thrombolysis: synthetic tissue plasminogen activator (eg Alteplase)- clotbusting drug
Contraindications: (neurosurgery last 3 months, active internal bleeding etc)
NIH stroke scale: consider if score between 5 and 26
Timeframe: within 4.5 hours (thrombolysis window) Limited benefit beyon this time with increased bleeding risk
If thrombolysis is not appropriate, start immediately on 300mg of aspirin for two weeks, after two weeks, conversion to secondary prophylaxis with 75mg clopidogrel is indicated unless anti-coagulation is appropriate because of aetiology
If thrombolysis was given, aspirin is usually started 24-48 hours following treatment
Thrombectomy:
Removal of thrombus from a vessel
Ongoing management: Admission to a hyperacute stroke unit for ongoing monitoring is essential BP control Blood glucose control Anti-lipid therapy Anti-platelet/ anti-coagulation Carotid artery assessment Swallow and nutrition assessment Rehabilitation Palliative care
15
Q
What are potential complications following a stroke
A
Early: Haemorrhagic transformation of ischaemic stroke Cerebral oedema Seizures Infection (e.g. aspiration pneumonia) Cardiac arrhythmias Venous thromboembolism Death
Late: Mobility & sensory issues Bladder & bowel dysfunction Pain Fatigue Cognitive problems Visual problems Emotional and psychological issues Issues with swallowing, hydration and nutrition
16
Q
What is the prognosis of stroke
A
4th leading cause of death in Uk
1/7 patient with acute stroke die in hospital
~40& will have ongoing difficulties with basic activities of daily living 6 months after their stroke
17
Q
What is a sub-arachnoid haemorrhage
A
Bleeding into the subarachnoid space, where the cerebrospinal fluid is located, between the pia mater and the arachnoid membrane
18
Q
Who is most affected by sub-arachnoid haemorrhage
A
Black patients
Female
Age 45 to 70
19
Q
What causes a sub-arachnoid haemorrhage
A
Usually the result of a ruptured cerebral aneurysm
20
Q
What are the risk factors for a sub-arachnoid haemorrhage
A
Hypertension Smoking Excessive alcohol consumption Cocaine use Family history Sickle cell anaemia Marfan syndrome Ehlers Danlos syndrome Neurofibromatosis
21
Q
How does a sub-arachnoid haemorrhage present
A
Sudden onset occipital headache (AKA thunderclap headache) that occurs during strenuous activity such as weight lifting or sex
Described like being hit really hard on back of the head
Neck stiffness
Photophobia
Neurological symptoms such as visual changes, speech changes, weakness, seizures and loss of consciousness
22
Q
How is a sub-arachnoid haemorrhage investigated
A
Immediate CT head
Blood will cause hyperattenuation in the subarachnoid space
Normal CT does not always exclude diagnosis
Lumbar puncture
Collect a sample of CSF if CT head is negative
Raised red cell count
Xanthrochromia (yellow coloured CSF caused by bilirubin
Angiography
CT or MRI can be used once a subarachnoid haemorrhage is confirmed to locate the source of the bleed
23
Q
How is a sub-arachnoid haemorrhage treated
A
Managed by specialist neurosurgical unit
Those with reduced consciousness may require intubation and ventilation
Supportive care with nursing, nutrition and physiotherapy and occupational helath is needed throughout
Surgical intervention may be used to treat aneurysms, with the aim to repair the vessel and prevent further bleeds
Can be done through coiling, inserting a catheter into the arterial system, placing platinum coils in the aneurysm and sealing it off fromt he artery
An alternative is clipping, which involves cranial surgery and putting a clip on the aneurysm to seal it
Nimodipine is a calcium channel blocker that is used to prevent vasospasm- a common complication that can result in brain ischaemia following an SAH
LP or insertion of a shunt may be needed to treat hydrocephalus
Anti-eleptics can be used to treat seizures
24
Q
What is the prognosis of a sub-arachnoid haemorrhage
A
Very high mortality and morbidity
25
What is peripheral neuropathy
Damage or disease affecting the peripheral nerves - mononeuropathy or polyneuropathy or mononeuritis multiplex (several separate mononeuropathies)
Can be acute or chronic
26
What causes peripheral neuropathy
Diabetes is the most common cause
```
Causes of Peripheral Neuropathy:
A-lcohol and autoimmune diseases
B-12 deficiency
C-ancer and chronic kidney disease
D-iabetes and drugs (eg isoniazid, amiodarone and cisplatin)
E-very vasculitis
```
27
How does peripheral neuropathy present
Clove and stocking distribution is the classic sign of peripheral neuropathy
```
Sensory neuropathy - Diabetes, leprosy
Negative symptoms:
-Numbness/ pins and needles (extreme leads to loss of ability to feel pain)
-Tremor
-Gait abnormality
-Loss of temperature change detection
-Loss of coordination leading to loss of joint position sense
-Loss of ankle/knee jerks
Positive symptoms:
-Tingling
-Pain - burning or shooting pain (can be severe)
-Itching
-Crawling
-Pins and needles
```
```
Motor neuropathy - Guillain-Barre syndrome, Charcot-Marie-Tooth syndrome
Negative symptoms:
-Weakness - distal muscles of hands/feet (ie foot/wrist drop)
-Tiredness
-Heaviness
-Gait abnormalities
-Reduced reflexes
-Respiratory difficulty
-Muscle wasting
-Muscle paralysis
Positive symptoms:
-Cramps/myalgia
-Tremor
-Fasciculations
-Muscle twitching
```
Diabetic/Polyneuropathy - autonomic neuropathy
- Dizziness and fainting (because of lack of blood pressure control, leading to low blood pressure)
- Problems with sweating - reduced ability to sweat
- Inability to tolerate heat
- Loss of control over your bladder function - incontinence of urine
- Dysphagia, bloating, constipation or diarrhoea
- Inability to achieve an erection (impotence)
- Postural hypotension
- Abnormal pupillary dilation/ contriction
- Horner's syndrome - miosis, anhidrosis, ptosis
28
How is suspected peripheral neuropathy diagnosed
Diagnosis made mainly from detailed history and neuro examination
Blood tests: FBC, ESR, glucose, HbA1C, U and Es, LFT, TFT, B12, folate
Urine: glucose/protein
Genetic tests
Lead levels
Immunology: antibodies (eg intrinsic factor and gastric parietal cell antibody for Pernicious anaemia)
Nerve conduction studies
Electromyography
Nerve biopsy
Skin biopsy
MRI
LP (assesses possibiltiy of Guillain-Barre)
29
How is peripheral neuropathy treated
Treatment depends on cause
Physio/ occupational therapy/ Podiatrist:
- Walking aids
- Wheelchair
- Foot care
Pain management:
- Strategies to cope with pain - referral to pain management services
- Pharmacological treatment of neuropathic pain:
- - Amitriptyline
- - Nortriptyline
- - Gabapentin
- - Pregabalin
Treat the cause (eg diabetes or B12 deficiency)
Steroids
Reduced alcohol/carbs intake
For most types of neuropathy, no treatemnt is available that can cure or modify the disease. inthese cases, treatments are available for the symptoms of the disease especially pain.
- Analgesics
- Antidepressants
- Capsaisin gel
- Splints
- Surgery (decompression) - chronic symptoms, neurodeficit, Wallerian degeneration
30
What are potential complications of peripheral neuropathy
Depression
Permanent nerve damage
Social isolation/ breakdown of relationships due to impact of chronic pain
31
What is the prognosis for peripheral neuropathy
High mortality and morbidity rate (especially in DM)
Permanent joint destruction and nerve damage
Disability, social isolation, loss of independence
32
What is epilepsy
Epilepsy is an umbrella term for a condition where there is a tendancy to have seizures
Seizures are transient episodes of abnormal electrical activity in the brain
There are many types of seizure
A diagnosis of epilepsy is made by a specialist based on the characteristics of the seizure episodes
33
What are the types of epilepsy
```
Generalised tonic clonic seizures
Focal seizures
Absence seizures
Atonic seizures
Myclonic seizures
Infantile spasms
```
34
What are the features of generalised tonic clonic seizures
Episodes of:
-Loss of consciousness
-Tonic (muscle tensing)
-Clonic (muscle jerking)
Typically the tonic phase comes before the clonic phase
May be associated tongue biting, incontinence, groaning and irregular breathing
After the seizure there is a prolonged post-ictal period where the person is confused, drowsy and irritable or depressed
35
What are the features of focal seizures
```
Start in the temporal lobes
Affect hearing, speech, memory and emotions
Can present as:
-hallucinations
-memory flashback
-Deja vu
-Doing strange things on autopilot
```
36
What are the features of absence seizures
Typically occur in children
Patient becomes blank, stares into space and then abruptly returns to normal
During the episode they are unaware of their surroundings and won't respond
Typically only lasts 10 to 20 seconds
Most patients (>90%) stop having these as they get older
37
What are the features of atonic seizures
AKA drop attacks
Characterised by brief lapses in muscle tone
Don't usually last more than 3 minutes
Typically begin in childhood
May be indicative of Lennox-Gastaut syndrome
38
What are the features of myoclonic seizures
Present as sudden brief muscle contractions, like a sudden jump.
Patient usually remains awake during the episode
Occur in various forms of epilepsy but typically happen in children as part of juvenile myoclonic epilepsy
39
What are the features of infantile spasms
AKA West syndrome
It is rare (1 in 4000) disorder starting in infancy at around 6 months of age
It is characterised by clusters of full body spasms
Poor prognosis 1/3 die by the age of 25, however 1/3 are seizure free
40
How is suspected epilepsy investigated
An electroenchephalogram (EEG) can show typical patterns in different forms of epilepsy and support the diagnosis
An MRI brain can be used to visualise the structure of the brain and is used to diagnose structural problems that may be associated with seizures and other pathology such as tumours
ECG can be used to exclude any heart problems accompany the diagnosis
41
How are generalised tonic-clonic seizures treated
First line: sodium valproate
| Second line: lamotrigine or carbamazepine
42
How are focal seizures treated
The reverse of tonic clonic seizures:
First line: lamotrigine or carbamazepine
Second line: sodium valproate or levetiracetam
43
How are absence seizures treated
First line: sodium valproate or ethosuximide
44
How are atonic seizures treated
First line: sodium valproate
| Second line: lamotrigine
45
How are myoclonic seizures treated
First line: sodium valproate
| Other options: lamotrigine, levetiracetam or topiramide
46
How are infantile spasms treated
Prednisolone
| Vigabatrin
47
What are the epilepsy maintenance medications
```
Sodium Valproate
First line option in most forms of epilepsy
Works by increasing the activity of GABA, which relaxes the brain
SIde effects:
-teratogenic
-liver damage or hepatitis
-hair loss
-tremor
```
```
Carbamazepine:
First line for focal seizures
Side effects:
-agranulocytosis
-aplastic anaemia
-induces the P450 system so there are many drug interactions
```
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Phenytoin:
Side effects:
-folate and Vit D defficiency
-Megoblastic anaemia
-Osteomalacia
```
Ethosuximide:
Side effects:
Stevens-Johnson syndrome or DRESS syndrome (life threatening skin rashes
-Leukopenia
48
What is status epilepticus
Status epilepticus:
A medical emergency
Seizures lasting more than 5 minutes or more than 3 seizures in one hour
Management (take an ABCDE approach)
- Secure the airway
- Give high-concentration O2
- Assess cardiac and respiratory function
- Check blood glucose levels
- Gain IV acess (insert a cannula)
- IV lorazepam 4mg, repeated after 10 minutes if the seizure continues
- If seizures persist give IV phenobarbital or phenytoin
Medical options in the community:
- Buccal midazolam
- Rectal diazepam
49
What is meningitis
Inflammation of the meninges, which are the lining of the brain and spinal cord.
50
What is meningococcal septicaemia
When the meningococcus bacterial infection is in the blood stream. This is the cause of the classic non-blanching rash that everybody worries about. This rash indicates has caused disseminated intravascular coagulopathy and subcutaneous haemorrhages.
Neisseria meningitidis is a gram negative diplococcus bacteria. They are circular bacteria (cocci) that occur in pairs (diplo-). It is commonly known as meningococcus.
51
What is meningococcal meningitis
When the meningococcus bacteria is infecting the meninges and the cerebrospinal fluid around the brain and spinal cord.
52
How common is meningitis
~1.2 million cases worldwide each year
53
What causes meningitis
The inflammation is usually due to a bacterial or viral infection.
Bacterial meningits is inflammation of the meninges caused by a bacterial infection. Most commonly by:
- Neisseria meningitidis (meningococcus)
- Streptococcus pneumoniae (pneumococcus)
- Group B Streptococcus (in neonates) - usually contracted during birth from GBS bacteria that often lives harmlessly in the mother's vagina
54
What are the risk factors for meningitis
```
Advanced age
Crowded populations
Exposure to pathogens
Immunocompromised
Cranial anatomoical deficits
Cochlear implants
Sickle cell disease
Contiguous infections
```
55
How does meningitis present
```
Fever
Neck stiffness
Vomiting
Headache
Photophobia
Altered consciousness
Seizures
Non-blanching rash (in meningococcal septicaemia)
```
Neonates and babies can present with very non-specific signs and symptoms:
- hypotonia
- poor feeding
- lethargy
- hypothermia
- a bulging fontanelle
56
What are the differentials in suspected meningitis
```
Encephalitis
Drug induced meningitis
Tuberculosis meningitis
Fungal meningitis
Viral meningitis
Bacterial meningitis
```
57
How is suspected meningitis investigated
Lumbar puncture as part of investigation in all children:
- Under 1 months presenting with fever
- 1 to 3 months with fever and are unwell
- Under 1 years with unexplained fever and other features of serious illness
Two special tests for meningeal irritation:
- Kernig's test:
- - Lie patient on their back
- - Flex one hip and knee to 90 degrees
- - Slowly straighten the knee, keeping hip flexed at 90 degrees
- - This creates a slight stretch in the meninges
- - Where there is meningits, it will produce spinal pain or resistance to this movement
- Brudzinski's test:
- - Lie patient on their back
- - Gently use your hands to raise their head and neck off the bed, flexing their chin to their chest
- - A positive test is when this causes the patient to involuntarily flex their hips and knees
58
How is meningitis treated
Meningococcal septicaemia and bacterial meningitis are medical emergencies and should be treated immediately
Community:
Those with suspected meningitis and a non-blanching rash should recieve an urgent stat injection (IM or IV) of benzylpenicillin prior to transfer to hospital (see page 158 of zero to finals for dose)
If there is a true penicillin allergy, transfer should be the priority rather than other antibiotics
Hospital:
Ideally take a blood culture and do an LP for CSF beofre starting antibiotics but if pt is acutely unwell, do not delay treatment.
Send blood tests for meningococcal PCR if meningococcal disease is suspected, this tests directly for the meningococcal DNA.
Should have a low threshold for treating suspected bacterial meningitis, particularly in babies and young children.
Treat with abx in accordance with local guidelines. Typically:
-Under 3 months - cefotaxime plus amoxicillin
-Above 3 months - ceftriaxone
Vancomycin can be used if penicillin resistent pneumococcal infection, for example from recent foreign travel or prolonged antibiotic exposure
Steroids can be used in bacterial meningitis to reduce the frequency and severity of hearing loss and neurological damage:
-Dexamethosone, gievn 4 times daily for 4 days to children over 3 months if LP is suggestive of baceterial meningitis
Bacterial meningitis and meningococcal infection are notifiable diseases, so public health need to be informed of all cases.
Significant exposure to a pt with meningococcal infections puts people at risk of contracting the illness themselves, with the risk being highest for those who had close prolonged contact withing the 7 days prior to the onset of symptoms in the pt.
The risk of developing this disease decreases 7 days after the exposure, so if no symptoms have developed by this time, it is unlikely they will develop the illness.
Post exposure prophylaxis is guided by public health. Usual abx used is a single dose of ciprofloxacin, given as soon as possible, ideally within 24 hours of the initial diagnosis.
A sample of the CSF from the LP should be sent for viral PCR testing.
Viral meningitis tends to be milder than bacterial and often only requires supportive treatment.
Aciclovir can be used to treat suspected or confirmed HSZ meningitis.
See page 159 of zero to finals for LP interpretation."
59
What are the potential complications go meningitis
- Hearing loss (key)
- Seizures and epilepsy
- Cognitive impairment and learning disabilities
- Memory loss
- Focal neurological deficits suchas limb weakness or spasticity
60
What is a migraine
A complex neurological condition that cause headache and other associated symptoms.
They occur in attacks that often follow a typical pattern.
61
What are the types of migraine
- Migraine without aura
- Migraine with aura
- Silent migraine (aura wihtout a headache)
- Hemiplegic migraine
62
What are the five stages along the course of a migraine
The course of a migraine can be described in 5 stages. Not typical of everyone and will vary between patients, with some only experiencing one or two of the stages.
- The prodromal stage: can involve several days of subtle symptoms (yawning, fatigue or mood changes) prior to onset of the migraine
- Aura (lasting up to 60 minutes)
- Headache (last 4 to 72 hours)
- Resolution (the headache can fade away or be relieved completely by vomiting or sleeping
- Postdromal or recovery
63
What causes migraines
No simple explanation for why migraines occur but is believed to be a combination of structural, functional, chemical, vascular and inflammatory factors
Can have specific triggers that are individual to the person, that are often not possible to identify triggers. Potential triggers are:
- stress
- bright light
- strong smells
- certain foods (eg chocolate, cheese and caffeine)
- dehydration
- menstruation
- abnormal sleep patterns
- trauma
64
How do migraines present
Typical headache symptoms:
- last between 4 to 72 hours
- moderate to sever intensity
- pounding or throbbing in nature
- usually unilateral but can be bilateral
- photophobia
- phonophobia
- with or without aura
- nausea and vomiting
Aura:
- term used to describe the visual changes associated with migraines
- multiple types:
- - Sparks in vision
- - Blurred vision
- - Lines across vision
- - Loss of different visual fields
Hemiplegic migraine:
- can mimic stroke
- essential to act fast and exclude a stroke in pts presenting with symptoms of HM
- typical migraine symptoms
- sudden or gradual onset
- Hemiplegia (unilateral weakness of the limbs
- Ataxia (off balance)
- changes in consciousness
65
What should be discussed with migraine patients
Keeping a headache diary can be helpful in identifying the triggers.
Avoiding triggers can reduce the frequency of the migraines
Also useful in demonstrating the response to treatment
66
How are migraines managed
Acute management:
- often patients will go to a dark quiet room and sleep
- medical management are:
- - paracetamol
- - triptans (sumatriptan 50mg as the migraine starts)
- - NSAIDs (ibuprofen or naproxen)
- - Anti-emetics if vomiting occurs (metoclopramide)
Triptans are used to abort migraines when they start to develop. They are 5HT receptors agonists (serotonin receptor agonists). They various mechanisms of action and it is not clear which mechanisms are responsible for their effects on migraines. They act on:
- Smooth muscle in arteries to cause vasoconstriction
- Peripheral pain receptors to inhibit activation of pain receptors
- Reduce neuronal activity in the central nervous system
Long-term medication:
- Propranolol
- Topiramate
- Amitriptyline
Acupuncture recommended by NICE
Supplementation with Vit B2 (riboflavin) may reduce frequency and severity of attacks
67
What is the prognosis of migraines
Tend to get better over time and people often go into remission from their symptoms
68
What are tension headaches
Tension type headaches can be either episodic or chronic.
They are rarely disabling or associated with any significant autonomic phenomena, thus patients do not usually seek medical care and usually successfully self-treat.
The attacks are generalised throughout the head with a predilection for involving the frontal and occipital regions.
The pain is typically expressed as being a tight band around the head.
It does not worsen with routine physical activity"
69
How common are tension headaches
Most common type od headache
The mean global prevalence in adults is 42%
Chronic type occurs in 2% to 3% of the population.
70
Who do tension headaches affect
Onset is generally between 20 to 30 y/o, with prevalence peaking between 20 and 39 and then declining.
Only slightly more common in females with a 2:3 male to female ratio
71
What causes tension headaches
Muscle contraction often considered the cause but little evidence to support this.
Psychological stress is the most common trigger
Disturbed sleep patterns can trigger an episodic tensiontype headache
Insomnia and other sleep disorders are associated with chronic tension type headache
72
What are the risk factors for tension headaches
Strong:
- Mental tension
- Stress
- Missing meals
- Fatigue
Weak:
- Somatisation
- Female sex
- Age 20-39 y/o
- Lower socioeconomic status
- Analgesic overuse
73
How do tension headaches present
Common:
- Generalised head pain
- Frontal or occipital head pain
- Non-pulsatile head pain
- Constricting pain
- Normal neurological examination
- Pericranial tenderness
- Strenocleidomastoid muscle tenderness
- Trapezius muscle tenderness
- Temporalis muscel tenderness
- Lateral pterygoid muscle tenderness
- Masseter muscle tenderness
Uncommon:
- Photophobia
- Phonophobia
- Regular analgesic use
- Anxiety
- Depression
- Somatisation
74
What are the differentials of suspected tension headache
```
Chronic migraine
Medicine overuse headache
Sphenoid sinusitis
Giant cell arteritis
Temporomandibular disorder (TMD)
Pituitary tumour
Brain tumour
Chronic subdural haematoma
Pseudotumor cerebri (idiopathic intracranial hypetension)
Cervical pathology
```
75
How are tension headaches treated
Goal is to reduce the discomfort and duration of attacks
Usually episodic is successfully self-treated
Acute:
Simple analgesics (paracetamol, NSAIDs)
Treatment should be at early onset of attack
Ideally avoid butalbital medications due to risk of developing medication overuse headache
If frequency of attacks increases, stronger analgesics have limited use due to disk of transformation into chronic headache, potentially due to medicine overuse syndrome (aka analgesic rebound) where the analgesics cease to provide pain relief and perpetuate and intensify the headaches
Sometimes a pt will require parenteral meds (eg antiemetics, analgesics) for treatment, having failed on simple analgesics
Preventative treatment:
Used when patients experience greater than 7 to 9 headache days per month
Low-dose tricyclic antidepressants may reduce frequency and intensity of attacks (eg amitriptyline)
Little evidence to support the use of muscle relaxants in the management of tension-type headaches, but may be used as second-line medication (Tizanidine can be used for 3-6 months then stopped, if symptoms return the further Tizanidine may be appropriate)
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Non-drug treatment:
-Relaxation training
-CBT
-Myofascial trigger point-focused massage
-Electromyographic biofeedback
-Physiotherapy
-Acupuncture
-Spinal manipulation
-Hypnosis
Can be used as adjuncts to drug treatments
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If standard treatments fail, diagnosis should be reconsidered
76
What is the prognosis for those with tension headaches
Most common type of headache in the general population
Most common between ages of 20-39 years and then decline
Self treatment is usually effective
Potential of peptic ulcer complication
77
What is Parkinson's disease
A condition where there is progressive reduction of dopamine in the basal ganglia of the brain, leading to disorders of movement
78
Who is most affected by Parkinson's disease
Age>70
| Male
79
What causes Parkinson's disease
The basal ganglia are a group of structures situated in the middle of brain.
They are responsible for coordinating habital movements such as walking or looking around, controlling voluntary movements and learning specific movement patterns
Part of the basal ganglia called the substantia nigra, produces a neurotransmitter called dopamine, which is essential for the correct functioning of the basal ganglia.
In Parkinson's disease, there is a gradual but progressive fall in the production of dopamine
80
What are the risk factors for Parkinson's disease
```
Age
Male
Head trauma
Family history
Exposure to toxins (eg herbicides and pesticides)
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How does Parkinson's disease present
Symptoms are characteristically asymmetrical, with one side affected more than the other
Classic triad:
- Resting tremor
- Rigidity
- Bradykinesia
Unilateral tremor:
- occurs 4 to 6 times a second (4-6Hz)
- described as a pill rolling tremor because it looks like they are rolling a pill between their fingertips and thumb
- more pronounced when resting and improves on voluntary movement
- worsens when the patient is distracted
- asking them to do a task with the other hand can exaggerate the tremor
Cogwheel rigidity:
a resistance to passive movement of a joint
Bradykineasia:
- slower and smaller movements
- handwriting gets smaller and smaller
- can only take small steps when walking (shuffling gait)
- difficulty initiating movement
- difficulty turning around when standing, have to take lots of little steps
- reduced facial movements and expressions (hypomimia)
Other features:
- depression
- sleep disturbance and insomnia
- loss of sense of smell (anosmia)
- postural instability
- cognitive impairment and memory problems
See page 280 of zero to finals book for table on difference between Parkinson's and Benign Essential tremors
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What other conditions may present similarly to Parkinson's disease
Multiple system atrophy
Dementia with Lewy Bodies
Progressive Supranuclear Palsy
Corticobasal Degeneration
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How is Parkinson's disease diagnosed
Diagnosed clinically based on symptoms and examination
Should be diagnosed by a specialist with experience diagnosing Parkinson's
NICE recommend using the UK Parkinson's Disease Society brain bank clinical diagnostic criteria
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How is Parkinson's disease treated
Treatment should be under a specialist
No cure and so the treatment is focused on controlling symptoms and minimising side effects
Patients describe themselves as ""on"" when the medications are acting and they are moving freely, and ""off"" when the medications wear out, they have significant symptoms and their next dose is due
Medications:
Levodopa: a synthetic dopamine given orally to boost dopamine levels. It is usually combined with a drug that stops levodopa being broken in the body before it gets the chance to enter the brain.
These are peripheral decarboxylase inhibitors (eg carbidopa, and benserazide)
Comination drugs are:
- Co-benyldopa (levodopa and benserazide)
- Co-careldopa (levodopa and carbidopa)
COMT inhibitors (eg entacapone)
Dopamine agonists (eg Bromocryptine)
Monoamine Oxidase-B inhibitors (eg Selegiline)
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What is a risk of Parkinson's treatment
Main side effect of dopamine is when the dose is too high patients develop dyskinesias. These are abnormal movements associated with excessive motor activity. Examples are:
- Dystonia - excessive muscle contraction leads to abnormal postures or exaggerated movements
- Chorea - abnormal involuntary movements that can be jerking and random
- Athetosis - involuntary twisting or writhing movements usually in the fingers, hands and feet
