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Thanks to any who have managed to visit this site after 17th June. Use the categories menu on the left or the search box to find what you were looking for. If you select Category- Primary Care Neurology you will see summaries of all posts related to the Primary Care Neurology series.

If I remember, I was to post the following:

1. List of Migraine Prophylactic drugs
2. BASH Headache Guidelines
3. Forbes Quick Neurological Examination printable sheet for patient records
4. Forbes Quick Neurological Examination Video - has yet to be uploaded but the powerpoint version with audio can be viewed via authorstream.com

If there were any other queries - please email or leave a comment here.

I will upload the slides from Tuesday evening shortly.

Thanks

This is a short-cut examination, but I use this all the time or a variation of it, so I am not trying to fob you off with something half-baked or useless or dangerous. This is what neurologists do - spend time on the history, and target important positives or negatives. It emphasises normal or abnormal signs that would change management - “deal clinchers”. Usually the history will direct almost every clinical decision you make, but a screening examination that is easy to use is an important addition to your clinical skills.

If you don’t like reading and want to cut to the video (which will be online by 19th June)- visit Forbes Quick Neurological Examination
Authorstream.com have hosted a powerpoint version of the Forbes Quick Neurological Examination.
Here’s the 7 point summary:

1. Walk
2. Talk
3. Vision
4. Face
5. Upper Limb
6. Lower Limb
7. General Exam

Now here’s the detail:

1. Walk
   • Watch your patient walk into the room

Always see your patient walking. Someone who can walk normally into your room is unlikely to have serious disease of their brain, spinal cord or peripheral neuromuscular system i.e the parts of the brain that deal with locomotion

2. Talk
   • Listen to the history !

   By the time a history has been taken you will have judged the following elements of speech and language: comprehension, fluency, naming. If they can do this it is unlikely that you have missed a significant language problem.

3. Vision
   Ask if they have seen their optician recently. Anyone who has been to an opticians, been issued with a pair of glasses, and is satisifed with their vision is unlikely to have serious neuro-ophthalmological disease. If they have not been to an optician recently do the following:
   • Check acuity with Snellen Chart

   Remember to get the best possible vision with correction (glasses or pinhole)

   • Check Visual Fields

   The video of visual field test is easier than reading all this…Ask patient to look at your face. Lift your hands up, so that there is one in each peripheral field. Then extend the index finger of each hand. Ask the patient to look at your face and say how many fingers in TOTAL you have put up. The person is seeing correctly in their peripheral field if they say “2″ or you notice them making a quick eye movement to each side when they think you are playing a trick on them!

   • Check eye movements

   Check the short video of eye movement testing . Make sure the eyes can move all the way up and down and side to side. Internuclear ophthalmoplegia and trochlear nerve palsy are difficult to elicit - you should refer unless you are confident about what you are doing. Sustained, reproducible nystagmus in someone with neurological symptoms is significant - usually indicates brainstem disease (usually inflammation or infarction).

   • Ophthalmoscopy

   Papilloedema will always make a referral necessary - so check the discs! Remember to ask the patient to look into the distance, and then aim your ophthalmoscope towards the opposite mastoid process which is likely to bring the disc into view, or allow you to see a retinal vessel you can follow to the centre.

   • If in doubt - you could ask them to see their optician!
4. Face
   Examine facial muscles: Ask your patient to close their eyes as tightly as they can - ‘like there was soap in them’. Try and prise the eyes open. Then ask them close their lips as tightly as possible - again try to prise them open.
   • Eyelashes buried both sides, and not able to prise open = normal
   • Unable to prise lips open = normal

If the top and bottom half of the face are weak you are usually dealing with Idiopathic Facial Paralysis = Bell’s Palsy.
If you have isolated weakness of one side of the mouth you are probably dealing with a stroke - look at the nasolabial crease.

These videos made by a Canadian Lady with Bell’s Palsy illustrate the point beautifully. She gives the most eloquent decription of the symptoms and impact of Bell’s Palsy I have ever heard - we wish her well. Note how both eye and lip have difficulty closing:

5. Upper Limb
   Upper limb exam is summarised here.
   • Pronator Drift

   Hold arms out in front, and if they can hold their posture for 10 seconds with eyes closed, they are normal. My own video of how to test will appear here. Another pronator drift video can be viewed here.

   • Finger nose test

   After pronator drift, ask them to touch nose with each index finger - eyes can be open for this. The manoeuvre is called the finger-nose test. If this is done accurately, test is normal. An abnormal finger nose test is illustrated here using another of Dr Zerati’s cerebellar disease videos.

   • Test shoulder abduction

   This tests for upper motor neuron disease. See video of shoulder abduction.

   • Tendon reflexes
   • Tendon reflexes should be second nature, but only help in the upper limb if you suspect nerve root disease, which you will usually have diagnosed from the history, but I’ve included them here as it seems heretical not to. You can miss them out in a quick screen.
6. Lower Limb
   • Sitting on chair, test Hip Flexion

   Hip Flexion is the best test for upper motor neuron weakness of the lower limb. It is nearly always weak in significant spinal cord disease. The misused term “proximal myopathy” means that most people believe hip flexion weakness to be indicative of muscle disease, when it is most often spinal cord! If you test in the sitting position, you isolate the ilio-psoas muscle, which makes the test more sensitive, so you are more likely to reassure correctly if full strength is elicited.

   • Sitting on chair- test knee extension

   If you have normal hip flexion and normal knee extension - you can stand and should be able to walk with assistance.

   • Ankle jerk

   The ankle jerk is usually the first reflex to disappear in peripheral nerve disease. The most common reason for being absent is a helpful patient! They will try to assist you by actively dorsiflexing the foot (the tibialis anterior tendon will be prominent) which will make it impossible to get the ankle jerk to work. Watch the tibialis anterior tendon before you make your strike - ankle jerk video will help you identify this.

   • Plantar response

   Again lots of myths. Babinski discovered this reflex in 1800s - his clinical interest was hysteria, and he realised that toe extension caused by stroking the lateral aspect of the foot occurred consistently in organic disease. The reproducible extension of the great toe is the pathological feature. Don’t worry about fanning of toes, or split second toe flexion - an extensor plantar is reproducible. If you have someone with diffiulty walking and you find an extensor plantar, I have always said I would guarantee an urgent out-patient appointment to any (Southern Trust) GP for their patient as there must be something going on. See video on plantar response.

7. General Exam
   • In acute headache you may wish to look for Horner’s Syndrome (carotid dissection) or meningism (see video on additional reflexes and meningism , at about 1 minute after the start of the video, the doctor correctly tests for meningism)
   • In suspected cerebrovascular disease- pulse, BP, cardiac and carotid auscultation
   • Listen to chest and palpate abdomen and check for rash in suspected systemic illness - sorry I know this is common sense

This will depend upon your scenario.

The full Forbes Quick Neurological Exam video is here.

This is a list of serious neurological conditions which if unrecognised, will cause serious harm if misdiagnosed or undiagnosed. If diagnosed, there are effective, if not curative, treatments:

1. Myasthenia Gravis

Usually present with diplopia or ptosis or facial weakness. Anyone with diplopia should have their facial muscles tested . The combination of diplopia and facial weakness is almost always myasthenia. Most cases have postive acetylcholine receptor anti-bodies.

2. Hypnic Headache

This is a headache that exclusively wakens (the usually retirement aged patient) from sleep nearly every night. The pain may persists for several hours, and the patient may fear going to sleep knowing that the pain wil occur. Lithium at doses of 200-400mg can be highly effective.

3. Dysimmune neuropathies

Chronic inflammatory demyelinating polyneuropathy (CIDP), can cause insidious weakness in an elderly patient, who may quite happily accept the diability associated with “old age”. The clues are weak hip flexion muscles and absent relfexes, but almost no sensory component nor muscle wasting.

4. Wilson’s Disease

I’ve never diagnosed a case, but have inherited two cases from other neurologists- approx frequency is about 1 in 200,000. However, copper-chelating therapy can arrest neurological progression - I will test young onset movement disorders for serum copper and caeruloplasmin and if in doubt, 24 hour urinary copper excretion.

5. Segawa’s Disease

This is a rare type of cerebral palsy, with dystonic posturing of the lower limbs. It responds to levo-DOPA! I know of one case only, but it should be considered in young people with abnormal gaits attributed to CP.

6. Paroxysmal Kinisegenic Choreoathetosis

This disorder causes repeated involuntary movements in children and adolescents, and can be misdiagnosed as Tourette’s syndrome. It can be suppressed efectively with anti-convulsants such as Tegretol, Epilim or Lamotrigine etc.

There are others, but these are prominent. I’ll add to the list.

Here are my thoughts on prescribing in primary care. In many ways migraine is entirely a primary care subject, and a lot of excellent writing on migraine emanantes from general practice. Only 1-3% of headache cases from primary care ever get to an NHS Neurology clinic, so I see a lot less migraine than most general practitioners. However, here’s a few points:

1. Correct Diagnosis of Migraine

A short reminder on migraine diagnosis is worth repeating - episodic headaches of moderate-severe intensity associated with sensory sensitivity. Unsuccessful migraine treatment is often due to a mis-diagnosis, such as tension-type headache or more rarely cluster-type headache (the so-called trigeminal autonomic cephalalgias). Medication-overuse headache is the other diagnostic trap, and even though your prescribing pad is quiet, many over-the-counter preparations may contain enough codeine or caffeine to induce chronic medication overuse headache. If you are prescribing a lot of triptans for migraine (being used more than twice per week), you may have a triptan headache on your hands.

2. Don’t prescribe in migraine - tackle lifestyle

There is some reasonable scientific evidence behind lifestyle adjustment and improving migraine headache severity. Specifically, there is observational evidence on

1. Hydration
2. Stress avoidance
3. Weight management

Increased BMI is associated with more frequent headaches

4. Sleep hygiene
5. Exercise

Exercise is tricky - too much can provoke migraine in some people - especially if unaccustomed, but gentle exercise - walking is perfect- I’m sure is beneficial.

I’ve summarised these in a short article called 7 steps to treat migraine . This article is free to distribute. It is a summary of my own ideas on migraine treatment. (The other 2 steps outlined below are an effective acute treatment and an effective prophylactic treatment)

3. An effective acute treatment for migraine

The British Association for the Study of Headache has published guidelines on acute treatment of migraine and other headche disorders. Like many guidelines they are comprehensive and well researched, but difficult to access as an aide memoire. Here’s my suggested list for a drug naive patient:

• Aspirin 600-900 mg chewed and absorbed via buccal mucosa

Excellent RCT evidence: aspirin plus metoclopramide is equivalent to SC sumatriptan in migraine.

• Aspirin 600-900mg plus an anti-emetic like metoclopramide 10mg or buccal prochlorperazine 3-6mg

I’ve always been nervous about metoclopramide in migraine populations since seeing an oculo-gyric crisis, but the literature suggests that it is safe and effective, but buccal prochlorperazine seems a smarter option. Any NSAID can be used - specifically - ibuprofen, tolfenamic acid, naproxen - and all are probably more effective if used with an anti-emetic.

• Zomig rapimelts 2.5mg to 5mg

Don’t try these until you have had a go at the Aspirin / NSAID / anti-emetics. There is little to choose between any of the triptans. I use Zomig - they are licensed for use in adolescents - unlike other triptans. Rapimelts are absorbed effectively from the surface of the tongue.

4. Propranolol or Topiramate or Sodium Valproate for migraine prevention

These are my preferred prophylactic agents. There is RCT evidence to support their use, and a recent Cochrane review supports use of anti-convulsants in migraine prophylaxis.

The aim of the clinical examination is to exclude unsuspected serious disease. In migraine the risk of a serious intracranial abnormality is about 0.18%. This level is low enough to presume that the migraine is incidental, or that the diagnosis of migraine was incorrect!
I recommend Forbes Quick Neurological Examination, including checking blood pressure. Another useful tip is to palpate the scalp - you can identify trigger points over cutaneous nerves (which might be amenable to nerve blockade), and you can, in some people, reassure them, as they may be left with impression you have been thorough!

The diagnosis of migraine can be simply described:

1. Episodes of headache
2. Each headache episode is of moderate to severe intensity
3. Each headache is associated with sensory sensitivity

Sensory sensitivity is intolerance of light, noise, smell, movement, touch. Nausea is almost always present and vomiting can occur.

If you have these you have migraine. The clinical examination will exclude any serious alternative diagnosis. To meet these diagnostic guidelines in their strictest sense you should have had at least 3 such episodes of headache. As most people do not consult their doctors over headches, it is highly likely that anyone who does present will have had several headches in the past before deciding to see you.

Prescribing principles: Parkinsons Disease in Primary Care.
These are my thoughts on prescribing for Parkinson’s Disease in Primary care. They should reflect what I actually do, having considered evidence and guidelines alike.

1. Make sure that this is not just essential tremor

If your patient with tremor has essential tremor, then anti-parkinsonian treatment won’t work. In your examination, assess tone looking for rigidity and test repetitive movements looking for slowing of movement. If you have tremor, rigidity and bradykinesia, and it is predominantly one-sided, there is a fair chance this is indeed Parkinson’s Disease. If the tremor is the main problem and is symmetric, and there is no rigidity or bradykinesia, it is most likely to be essential tremor. For essential tremor I’d recommend beta-blockers - propranolol up to 80mg tid, Gabapentin up to 600mg tid, and there is some evidence for using Levetiracetam up to 500mg bd, or topiramate upto 100mg bd.

2. If you start treatment for Parkinson’s Disease, tell your patient there is a chance it may not work

The reason for this is that the clinical diagnosis of Parkinson’s can be incorrect in about 80-90% of cases. The conditions that mimic PD, such as small vessel cerebrovascular disease, MSA, PSP are a lot less likely to respond to levo-DOPA. However, if the PD diagnosis is correct, symptoms should improve on treatment. I, personally, have no objection to a general practitioner starting treatment in someone in whom they suspect Parkinson’s Disease, as long as they make thier patient aware of the diagnostic uncertainty. A referral to neurology/geriatrics is then appropriate. I disagree with the NICE guidance that everyone should be referred to a specialist and seen within 2 weeks - that is called de-skilling of general practice - no GP is going to start Levo-DOPA without significant consideration for their patient. I was recently asked by a Department of Health memo if “I complied with NICE guidance” - I don’t comply with guidance - it is guidance, not dictat! Its purpose is to provide information for us to weigh up and arrive at what we consider to be best care of our patients.

3. Start with a dopamine agonist, unless high risk arteriopath

The reason behind using dopamine agonists is to reduce the risk of late-levoDOPA syndrome. This is when people with PD start to experience unpredictable response to their medication and develop dyskinesia and freezing-gait episodes. However, this takes about 5 or more years to occur. Dopamine agonists are less potent than levo-DOPA. I try not to deny older people or high risk arteriopaths the benefit of levo-DOPA, so it is arguably inappropriate to start an arteriopath on dopamine agonists when the more potent drug should be given.

4. Keep treatment regimes simple

Aim for simple regimes of small doses given regularly. I am sceptical that a complex regime offers significant benefits over simpler ones. I often find in more complex cases changes in medication rarely lead to improvements. More important is to address a patients expectations of what is on offer. One situation which can, however, offer dramatic benefit, is the addition of amantadine to someone with severe dyskinesia.

5. If undertreated increase the dose

Once on anti-Parkinsonian medication, increases can be made. Increases in the total daily dose by 50 to 100mg of levo-DOPA are reasonable. Each step up can be made ona weekly basis, although more rapid increases can be tolerated. The main concerns in dose increases are

• postural hypotension
• nausea
• visual hallucinations
• confusion

If any of these occur, then you should reduce the dose. Domperidone is the preferred anti-emetic for nausea. Hallucinations are usually visual, the patient has insight and the most common ones observed are small animals in the corner of the room (Irish survey of 2007 suggested mice were number one visual hallucination in PD -this is true)!

To refresh your memory, here’s a fairly comprehensive list of Anti-Parkinsonian Medication
My frewquently used drugs are in bold:

1. Dopamine Agonists
• Ergot-derived
• Cabergoline
• Bromocriptine
• Pergolide
• Non-ergot derived
• Pramipexole
• Ropinirole
• Rotigozine
2. Levo-DOPA
• Sinemet
• Madopar
3. COMT-inhibitors
• Entacapone
• Stalevo is Entacapone 200mg and Sinemet in one tablet
• Tolcapone
4. MAOI-B
• Selegeline
• Rasagaline
5. Cholinesterase inhibitors
• Rivastigmine

Used in PD-related cognitive impairment.

Side-effects of PD medication
Nausea - any
Daytime sleepiness / sleep attacks - any
Visual hallucinations - any
Postural hypotension - any
Diarrhoea - COMTESS / STALEVO
Ankle oedema - Mirapexin
Cardiac valvulopathy - Cabergoline - I no longer use it or recommend it.

Other interventions in advanced cases. The aim of these interventions is to try and reduce the amount of fluctuation in motor control - so called “smoothing-out”.

1. Apomorphine subcutaneous infusion

I estimate that about 1-3% of PD cases may end up with an apomorphine pump - I have two after 4 years as a consultant neurologist.

2. APo-Go injector

I don’t use it, but some people may find it useful for people with unpredicatable freezing who can summon someone to administer it.

3. Deep brain stimulation

I only have one patient who has had deep brain stimulation in 4 years, who had previously been under the care of another neurologist elsewhere. Less than 0.1% of PD cases will end up with Deep Brain Stimulation at present.

There are several principles of prescribing in epilepsy that will help minimise error, yet optimise seizure control.
These principles are:

1. A correct diagnosis

The diagnosis of epilepsy should have been confirmed by a specialist with interest in epilepsy - usually a neurologist nowadays, but other experts include general physicians, geriatricians, learning disability psychiatrists and of course paediatricians. The main issue is that the specialist has taken the patient’s history and an eyewitness account, and these are both compatible with an epilepsy diagnosis. An EEG is not necessary for the diagnosis of epilepsy, especially if there is a structural lesion on imaging (such as a stroke, tumour, post-traumatic gliosis, or congenital defect).

2. A recurrent seizure is usually a recurrent seizure

If someone consults saying they have had another seizure - they are usually correct. However, you should always double check the history - people with epilepsy can faint, have dissociative events or attribute other symptoms to epilepsy, so it is always worth asking what they meant by “another seizure”.

3. Very frequent seizures in neurologically normal adults may not be epilepsy

One of the more frequent scenarios is that of non-epileptic attacks presenting as uncontrolled epilepsy. Neurologically normal individuals with a sudden “explosion” of seizure activity would be considered as possible cases of non-epileptic attacks and titration of anti-convulsants may not be appropriate. An enquiry about stressors may be more useful.

4. Non-Concordance is an important cause of recurrent seizures

The best way to test for non-concordance is to check a serum anti-convulsant level - although this is only widely available for carbamazepine, sodium valproate and phenytoin. However, it is an objective test for people in whom you doubt concordance.

5. If a recurrent seizure has occurred, and concordance is not an issue, increase the anti-convulsants

As a neurologist, I don’t in any way feel that I need to be consulted by a general practitioner about anti-convulsant titration. It is very hard to make any significant mistake that would compromise care of your patient. I normally make the following increments in the total daily dose after a recurrent seizure:

• Carbamazepine 200mg
• Sodium Valproate 500mg
• Lamotrigine 50mg
• Levetiracetam 500mg
• Topiramate 50mg
6. Using Phenytoin

I like to reserve phenytoin for emergency use, but many people have successful longterm control. When increasing phenytoin, you need to remember its zero-order pharmacokinetics, and a small change of 25mg can suddenly make your patient phenytoin-toxic. If an adult reaches 300mg daily of phenytoin and you still do not have complete seizure control, I’d recommend switching to a less complicated drug from the list above. I try not to get bogged down in small increments and repeated serum level testing, when there are better drugs and phenytoin is best left in reserve for emergency use.

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More of Edward Dullards photos can be appreciated using www.Flickr.com

These presentations should prompt urgent assessment:

1. Acute Severe Maximal at Onset Headache
2. A First Epileptic Seizure
3. Acute weakness or dysphasia
4. Difficulty walking with an extensor plantar response

You will not overwhelm the secondary care system by referring these red flag symptoms as emergencies to hospital.

A very sudden severe, maximal at onset headache, as the best estimate of frequency is about 30-40 per 100,000 each year. Each one can be sent to A&E.

A first unprovoked epileptic seizure occurs in about 60 per 100,000 each year, of whom about 50% end up with a diagnosis of epilepsy. Every acute hospital should run a dedicated first seizure service.

Difficulty walking with an extensor plantar response is refered to me about once every two months. This is equivalent to about 2/100,000 per year.

The suspected TIAs (weakness or dysphasia) are usually refered to a vascular service, and I do not have a good handle on how often referrals are made or the diagnostic outcome. However, about one person out of every 100,000 each day will have a stroke.

The point is that these circumstances are probably fairly infrequent, but memorable, events in the life of a GP, but can justify immediate contact with secondary care services.

The common causes of tremor are:

1. Physiological tremor
2. Essential tremor
3. Medication related tremor
4. Parkinsonism
• Parkinson’s Disease
• Cerebrovascular Disease
• Alzheimers Disease
• Parkinson-plus Disorders
5. Psychological based tremor

The person with tremor should have the following considered:

1. ?Hyperthyroid
2. ? medication associated with tremor
• Thyroxine
• Beta-agonists
• Sodium Valproate
• Lithium
• Neuroleptics
3. relief with alcohol - essential tremor
4. family history - essential tremor
5. one-side more than other - Parkinson’s
6. associated balance problem or slowing up - Parkinsonism
7. impaired memory - neurodegeneration
8. Distractable - psychologically-based

These videos will demonstrate the common tremor disorders:
If your computer seems very slow - try watching movement disorder videos here .

Parkinson’s Disease:

PARKINSON'S DISEASE 3
28 Nov 2007 at 6:59pm



PARKINSON'S DISEASE 2
25 Nov 2007 at 3:03pm




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Essential Tremor

(these are very severe examples however)


Tremor Action Network-Shaking the World
5 Jul 2007 at 8:02pm




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The differential diagnosis of a syncopal episode is:

1. Simple Faint
2. Cardiac Syncope
3. Seizure (epileptic seizure)
4. Uncertain cause
5. Non-epileptic seizure (psychologically based episodes)

If you are armed with this differential, and know the clinical features of each, you then take the history from the patient and reliable eye-witness. This history needs to be a blow-by-blow acocunt from the point the person was last normal, right through the prodrome, event itself, after the event until complete recovery.
Certain past or family history can be helpful:

• fainting can run in families, as can epilepsy
• Prior brain insult of any type is a risk factor for epilepsy
• Skull fracture
• Meningitis
• Febrile convulsion in infancy
• Stroke
• Cerebral Palsy, or congenital defect
• Cardiac Syncope usually occurs with known cardiac disease - usually ischaemic
• Non-epileptic seizures can be strongly associated with psycho-social stressors
• The usual reason for not making a diagnosis is lack of an eye-witness

Fainting
remember - Posture, Provocation, Prodrome and Pallor

Cardiac Syncope
No warning, except maybe brief light-head or palpitation. Rapid loss of awareness and rapid recovery.

Seizure
May call out at start of have focal onset symptoms (such as head-turning, stiffening of one arm only), then there is a 30-60 secdond tonic phase of marked rigidity, followed by a 3–60 second convulsive phase with clonic movements of the limbs. Eyes may be open, staring and face contorted. If the tongue is caught between the teeth, lateral tongue biting can occur. Incontinence can occur in any cause of syncope or seizure. During a seizure breath-holding - apnoea- is frequent and eye-witnesses often say they thought the person had died. A seizure usually lasts about 120 seconds, and there is usually very obvious confusion afterwards lasting many minutes.
This is a video, posted on Youtube of an epileptic seizure:

If the video is slow to load it may be quicker here: Epilepsy Video :

Graphic Epileptic Seizure
8 Sep 2007 at 2:32pm



Graphic Epileptic Seizure Footage
12 Jan 2007 at 8:07am




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Non-epileptic attacks
These are usually very prolonged, the patient may regain consciousnes in between episodes of atypical shaking and there is often no significant confusion afterwards. Head shaking from side-to-side, pelvic thrusting type movements, resisting eye-opening and directed agression are felt to be characteristic, but the diagnosis is a difficult one to make. There are vdieos on YouTube of people deliberately faking seizures (as a sick practical joke), but I can’t locate any genuine non-epileptic attacks yet.

I prefer the term altered sensation to “numbness” or “paraesthesia” as there are so many different types of altered sensation. I would recomend the “Basics” article on Altered Sensation”.
Briefly, the top causes are:

1. Migraine sensory aura
2. Carpal Tunnel Syndrome
3. Diabetic or alcoholic polyneuropathy

MS is a very rare cause of numbness. I estimate that only 3% of people refered to me with altered sensation will end up with a diagnosis of MS.

Briefly, the overwhelming majority of headache are benign. As a GP, the statistics are in your favour to not miss serious pathology. Only 2% of brain tumours willl present with headache as an isolated symptom. Brain tumours occur in 13/100,000 per annum, so you can do the stats to see that the occurence of a headache due to brain tumour is really small.
Prospective studies of migraine suggest an overall serious abnormality rate of 0.18%, and the lesions detected in these studies were incidental and equal to the baseline risk in any population, so the relationship with any associated headache is debatable.
The top 4 common headaches are:

• Tension-type headache
• Migraine
• Ice-pick headaches
• Medication overuse headache

Migraine is distinguished by its episodic nature, and more intense severity (disrupts normal activity) and its association with sensory sensitivity - especially nausea, and photophobia.
Tension-type headache is invariant, and pressure/tightness or dullness are described, and life usually carries on. Tension-type headache is associated with depression in some people.

Ice-pick pains are sudden intesne sharp pains that can occur in any area of the scalp. In some people they always occur in one location. The intensity of the pain is enough to either wince, scream or fall to the ground. After the brief, neuralgic pain a dull discomfort can linger for an hour or two. This is not a widely recognised symptom (I see a lot of this in out-patients and acute medical wards)

This video hosted by Dr Lipton (world famous headche specialist) can be played to hear more about the difference between migraine and tension-type headache:


Symptoms of Tension vs. Migraine Headache
28 Oct 2007 at 5:56pm




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There are other more serious headache presentations (temporal arteritis, subarachnoid haemorrhage, meningitis) which will be covered later.

I am extending the basic neurology to general practitioners, as I realise that the original course is really pitched at junior hopital doctors who aspire in hospital medicine.
I have created a category of “Primary Care” for these posts, so it should be possible to identify them easily. The syllabus is:

1. Overview of a Neurology Assessment in Primary Care
2. Common Symptoms
• Headache
• Numbness
• Syncope or Seizure
• Tremor
3. Red Flag Symptoms
• Acute Headache
• Seizure
• Difficulty walking
• Acute weakness
4. Forbes Quick Neurological Examination
• Walk
• Talk
• Vision
• Upper limb
• Lower Limb
• General Exam
5. Treating Common Neurological Problems
• Epilepsy
• Parkinson’s Disease
• Migraine
• Multiple Sclerosis
• Stroke
• Neuropathic pain

Specific questions can be forwarded here - please leave a comment - but you will need to register first - but do not fear - I will not misuse your email details.

I prefer to talk about Altered Sensation, a term that covers numbness (lack of sensation) paraesthesia (tingling) and altered perceptions of sensation such as allodynia (whenlight touch is painful). Other abnormal sensations include formication (a feeling like ants crawling over the skin), and people with spinothalamic tract lesions may describe sensations like “hot oil” in their bones. Burning pain can be reported too.

The approach to altered sensation is to try and establish to onset of the symptom the first time it occured. Remember the relationship between onset and pathophysiology?

In frequency terms the causes of numbness are:
1. Migraine sensory aura
2. Carpal tunnel syndrome
3. Diabetic polyneuropathy
4. Cervical radiculopathy
5. Cerebrovascular Disease
6. Focal brain or spinal cord inflammation

When eliciting a sensory history the keys are to (1) determine the territory affected and (2) determine the evolution of onset of an episode, and (3) find out if symptoms are episodic or not.

This leaves several combinations to narrow down the differential diagnosis:

• 1. Episodes of spreading numbness of face, upper limb or leg spreading over minutes and resoving within 30-90 minutes = migraine sensory aura
• 2. Episodes of numbness or tingling of one or both hands waking from sleep or occuring while driving - carpal tunnel syndrome
• 3. Numb feet, insidiously developing - polyneuropathy - alcohol or diabetes most comon aetiologies
• 4. Numbness or paraesthesia of one arm with some pain into the arm - cervical radiculopathy, constant over weeks or worse with neck movement
• 5. Instantaneous onset of numbness of one side of the body or unilatarally affecting one part of the body - cerebrovascular disease
• 6. Spreading numbness over days starting in one foot, spreading up one leg and then involving the other leg, developing over several days - inflammation of the spinal cord (myelitis) - if remitting the diagnosis is inflammation, if progressive spinal tumour will need to be considered

When is altered sensation due to Multiple Sclerosis?
The true answer is hardly ever! The diagnosis of MS requires discrete episodes of confirmed CNS inflammation affecting different areas of the brain, spinal cord or optic nerves. Newer criteria medicalise symptoms further by allowing a diagnosis at forst presentation - this is controversial for general neurologists like me. A first presentation of altered sensation at my neurology clinic probably has about a 1-3% chance of ending up with a diagnosis of Multiple Sclerosis within the next 10 years…. How do I work that out?
Altered sensation is about 20% of cases refered to me. If you remove those with the diagnoses listed 1-6 above, you are left with about 10 cases with a suspected CNS inflammatory lesion. About 5 of these will have a confirmed inflammatory lesion conformed on MRI. Of these the risk of recurrence (and therefore Multiple Sclerosis) is about 50% in the following 8 to 10 years. So about 2.5 of the original 100 people with altered sensation who attend me will end up with a Multiple Sclerosis diagnosis. If you are not practising in a neurology clinic, the probability of Multiple Sclerosis is even smaller!

The onset of a symptom is of extreme importance in neurology:

The following are generally true and if you stick to these mistakes are less likely. If you ever listen to a neurologist taking a history, he/she takes a lot of time eliciting the exact time of onset of a symptom and the evolution of a symptom.
Onset over:

1. Seconds - vascular, seizure
2. Minutes - migraine aura, vascular
3. Hours - inflammation, infection, migraine aura
4. Days - inflammation, infection
5. Weeks - inflammation, rapidly progressive tumour, chronic infection
6. Months - tumour, chronic inflammation, rapid degeneration
7. Years - genetic, neurodegenerative, slow growing tumour

There is overlap, but obviously a symptom occurring over seconds is not a neurodegenerative process! This framework should be committed to memory and with practice becomes intuitive.

Sometimes a careful history will prevent your patient from undergoing an unnecessary investigation. A common one is the person admitted with acute headache. The presenting complaint is “sudden severe headache”, and the label thunderclap headache is applied. The correct history may actually be..”all afternoon I had a mild, lingering discomfort in my head anf felt a bit sick. While driving home the headche became more intense. By the time I got into my house, the pain was excruciating. It was so bad I started to cry and my husband called an ambulance. I felt sick and had to lie down….” Get my drift?? This patient almost certainly has migraine, not subarachnoid haemorrhage and the lumbar puncture can be avoided.
Be very careful using the term “sudden”, try and get a prcise decription of onset - instead of thinking sudden, try and find out if it means instantaneous, or developing over minutes.

Acute headache comes in four varieties:

1. Acute Severe, Maximal at Onset (ASMO) also called “thunderclap”
2. Headache with Focal Neurology
3. New Persistent Headache
4. Headache with Fever

(1) Acute Severe Maximal at Onset - is exactly what it says (which is why I invented the term and encourage its use). I find the term thunderclap lacks description. The headache is one that is of almost instantaneous onset, maximal within no more than seconds, and can be global, or restricted to one area such as the occiput. Here’s the differential diagnosis, remembering that there is a 10-30% chance of detecting serious intracranial disease:

1. Idiopathic Thunderclap Headache
2. Subarachnoid haemorrhage
3. Cerebral venous sinus thrombosis
4. Other sudden increase of intracranial pressure
5. Sudden decrease of intracranial pressure
6. Pituitary Apoplexy
7. Cervical Arterial Dissection

These are the cases I have seen personally, so should do most people! There are rarer causes, and there is ongoing discussion on how much investigation should be done. I think that a normal CT Brain done within 24 hours and normal lumbar puncture with analysis of cerebrospinal fluid performed at least 12-16 hours after the onset of headache, and with opening pressure measures properly at LP will suffice. If these tests are normal but you clinically suspect another pathology such as carotid dissection then an MR angiogram could be performed.

(2) Headache with focal neurology
These are almost always migraine with aura. In my own series of over 80 prospectively collected cases, every one of those with headche and a focal neurological symptom had migraine with aura. remember these cases have presented with HEADACHE, but in the history you elicit blurred vision, numbnes or heaviness of a limb or face, or speech disturbance. Stroke is a cause of focal neurology with headache but the presentation in stroke is usually dominated by the focal neurology, not by the headache - about 30% of stroke patients will report headache.
In migraine aura, the hallmark is “SPREADING” of the disturbance. The physiology of migraine aura is thought to be “Leao’s spreading cortical depression”, where the cortex effectively switches off in a sustained depolarisation. This ‘electrical’ disturbance moves slowly across the cerebral cortex, and each new area involved will produce further symptoms. SO if your aura starts in the left occipital cortex, you get…..
….that’s right an evolving right homonymous hemianopia or visual aura, if it travels anteriorly into the parietal cortex … numbness or heaviness ensues. If it moves further forward into the frontal lobe paralysis or dysphasia will occur. The key fact in history is that there is a spreading of loss of function across adjacent cortical areas. Migraine aura can affect both occipital lobes and affect level of consciousness or provoke coma or vertigo (this relatively rare aura is called basilar migraine).
Here’s a video of a camerman’s impression of a migraine aura to give you an idea - it’s not usually quite so rapid:


Re: Scintillating Scotoma
17 Mar 2008 at 10:16am



Scintillating Scotoma
31 Mar 2007 at 8:37pm




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(3) New Persistent Headache
My differential diagnosis is

1. Systemic Illness Headache
2. Chronic migraine or tension-type headache with medication overuse
3. Spontaneous Intracranial Hypotension
4. Idiopathic Intracranial Hypertension
5. Cerebral venous sinus thrombosis
6. Carbon Monoxide poisoning
7. Sphenoid sinusitis
8. Temporal Arteritis
9. Medication toxicity
10. Pituitary Adenoma

This group of people either have a new headache that is not typical for migraine nor tension-type headache, but it is new and unusual for them. It may have features of raised intracranial pressure, in which case it is easy to realise they need a CT Brain and Lumbar puncture (with measurement of opening pressure!)
There may be systemic illness associated with these headaches, and temporal artieritis should be excluded in someone over the age of 50 years (a normal ESR usually suffices, but if there is diagnostic doubt a temporal artery biopsy is a small price to pay to prevent someone from ischaemic optic neuropathy).
Some people present with persistent daily headche and are at their “wits end”. These people will usually have either tension-type or migraine headche with associated medication overuse (”analgesic”) headache. A CT Brain is usually required for reassurance (NB incidental lesion rate is betwenn 1 and 7%), and medication withdrawal and migraine prophylaxis (Topiramate or amitryptiline or sodium valproate) should be used in conjunction with medication withdrawal.
Changes in intracranil presure can produce non-specific headaches, but you really need to have a postural element to convince me of a pressure related pain.
Sphenoid sinusitis can produce vague, centre of the head pains, and the sphenoid sinus can be overlooked if imaging is not carefully reviewed.
Pituitary disease can also cause headaches which are non-specific or have migrainous qualities.

(4) Headache and Fever
Differential diagnosis:

1. Systemic Illness headahe
2. Viral meningitis
3. Non-infectious aseptic meningitis
4. Bacterial meningitis

Cerebral abscess usually will present with focal neurology or seizure, and subdural empyema will occur in the context of recent craniotomy - it is theoretically possible for each to cause headche and fever without focal neurology or recent neurosurgery. Encephalitis will usually have seizures or confusion as a presenting complaint - the headache is not usually very severe or dominant.
Remember the correct technique for eliciting meningism - get your patient lying completely flat, and gently lift their head. Can’t find decent video for this - sorry.

Thats the history.

Go to Forbes’ Quick Neurological Examination.

This is the start of a short online course to help you practise neurology as a non-neurologist. There will be a mix of written material, videos and audio podcasts.
I will divide it into these sections:

1. Overview
2. Common Neurology Symptoms
• Acute Headache
• Suspected Seizure and Syncope
• Numbness
• Weakness
• Difficulty Walking
• Confusion
• Double vision
• Vertigo
• Tremor
3. Forbes’ Quick Neurology Examination
• Walk
• Talk
• Vision
• Face
• Upper Limbs
• Lower limbs
• General Examination
4. Writing a Differential Diagnosis
5. Using Neurology Investigations
• CT Brain
• MRI Spine
• Nerve Conduction
• EMG
• Lumbar Puncture
• Muscle Biopsy
• MRI Brain
• Brain biopsy
• Cerebral Angiography
6. Common Emergency Scenarios
• Status Epilepticus
• Coma
• Neurogenic Respiratory Failure
• Acute Confusional States
• Acute Stroke
• Spinal cord Compression

The emphasis will be on short articles to cope with short attention spans and will focus on key points. This will not be a comprehensive evidence based systematic review!
Expect updates daily.
Use the RSS feed to keep up to date: neurologyfeeds.com/feed.

NB: Please click on the title of this post if you do not see a long list of recent publications.

The latest headache publications from Cephalalgia, Headache and general neurology journals:

Subscribe to headache updates here

Cephalalgia

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Headache (American Headache Association)

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Journal of Neurology Neurosurgery and Psychiatry

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Annals of Neurology

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Neurology

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Lancet Neurology

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Brain: a journal of neurology

:
Migraine headache is not associated with cerebral or meningeal vasodilatation--a 3T magnetic resonance angiography study
by Schoonman, G. G., van der Grond, J., Kortmann, C., van der Geest, R. J., Terwindt, G. M., Ferrari, M. D.



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Archives of Neurology

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Journal of Neurology

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Latest publications from Movement Disorders, and filtered from general neurology journals:

Movement Disorders

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Journal of Neurology, Neurosurgery and Psychiatry

[Short reports] Transcranial sonography findings in a large family with homozygous and heterozygous PINK1 mutations
by Hagenah, J M, Becker, B, Bruggemann, N, Djarmati, A, Lohmann, K, Sprenger, A, Klein, C, Seidel, G



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Annals of Neurology

Characterization of PLA2G6 as a locus for dystonia-parkinsonism
by Coro Paisan-Ruiz, Kailash P. Bhatia, Abi Li, Dena Hernandez, Mary Davis, Nick W. Wood, John Hardy, Henry Houlden, Andrew Singleton, Susanne A. Schneider



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Neurology

Subthalamic nucleus stimulation in Parkinson disease: Exciting or depressing?
by Martin, W. R. W., Wieler, M.


STN-DBS activates the target area in Parkinson disease: An FDG-PET study
by Hilker, R., Voges, J., Weber, T., Kracht, L. W., Roggendorf, J., Baudrexel, S., Hoevels, M., Sturm, V., Heiss, W. D.



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Lancet Neurology

[Reflection and Reaction] The ancestry of LRRK2 Gly2019Ser parkinsonism
by Hani TS Benamer


[Reflection and Reaction] The ancestry of LRRK2 Gly2019Ser parkinsonism – Authors' reply
by Matthew J Farrer, Rachel Gibson, Fayçal Hentati



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Brain

The role of autophagy-lysosome pathway in neurodegeneration associated with Parkinson's disease
by Pan, T., Kondo, S., Le, W., Jankovic, J.


Parkinson's disease and dopaminergic therapy--differential effects on movement, reward and cognition
by Rowe, J. B., Hughes, L., Ghosh, B. C. P., Eckstein, D., Williams-Gray, C. H., Fallon, S., Barker, R. A., Owen, A. M.


A multitarget basal ganglia dopaminergic and GABAergic transplantation strategy enhances behavioural recovery in parkinsonian rats
by Mukhida, K., Hong, M., Miles, G.B., Phillips, T., Baghbaderani, B.A., McLeod, M., Kobayashi, N., Sen, A., Behie, L.A., Brownstone, R.M., Mendez, I.


Parthenogenetic dopamine neurons from primate embryonic stem cells restore function in experimental Parkinson's disease
by Sanchez-Pernaute, R., Lee, H., Patterson, M., Reske-Nielsen, C., Yoshizaki, T., Sonntag, K. C., Studer, L., Isacson, O.


Central and systemic IL-1 exacerbates neurodegeneration and motor symptoms in a model of Parkinson's disease
by Godoy, M. C. P., Tarelli, R., Ferrari, C. C., Sarchi, M. I., Pitossi, F. J.


Sensory deficit in Parkinson's disease: evidence of a cutaneous denervation
by Nolano, M., Provitera, V., Estraneo, A., Selim, M. M., Caporaso, G., Stancanelli, A., Saltalamacchia, A. M., Lanzillo, B., Santoro, L.



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Archives of Neurology

ORIGINAL CONTRIBUTION: Incidental Lewy Body Disease and Preclinical Parkinson Disease
by DelleDonne, A., Klos, K. J., Fujishiro, H., Ahmed, Z., Parisi, J. E., Josephs, K. A., Frigerio, R., Burnett, M., Wszolek, Z. K., Uitti, R. J., Ahlskog, J. E., Dickson, D. W.


BOOK REVIEWS: Parkinson Disease: Genetics and Pathogenesis
by Tan, E.-K.


EDITORIAL: Serum Uric Acid and Clinical Progression in Parkinson Disease: Potential Biomarker for Nigrostriatal Failure
by Schiess, M., Oh, I.


NEUROLOGICAL REVIEW: There Is No Parkinson Disease
by Weiner, W. J.


CLINICAL TRIALS: Serum Urate as a Predictor of Clinical and Radiographic Progression in Parkinson Disease
by Schwarzschild, M. A., Schwid, S. R., Marek, K., Watts, A., Lang, A. E., Oakes, D., Shoulson, I., Ascherio, A., and the Parkinson Study Group PRECEPT Investigators


ORIGINAL CONTRIBUTION: Mutation Analysis of the PINK1 Gene in 391 Patients With Parkinson Disease
by Kumazawa, R., Tomiyama, H., Li, Y., Imamichi, Y., Funayama, M., Yoshino, H., Yokochi, F., Fukusako, T., Takehisa, Y., Kashihara, K., Kondo, T., Elibol, B., Bostantjopoulou, S., Toda, T., Takahashi, H., Yoshii, F., Mizuno, Y., Hattori, N.


IMAGES IN NEUROLOGY: Postencephalitic Hemiparkinsonism: Clinical Imaging Correlation
by Hallevi, H., Oh, I. J., Valdez, S. R., Kidder, B. G., Schiess, M. C.


CORRESPONDENCE: The Need for Appropriate Genotyping Strategies for Glucocerebrosidase Mutations in Cohorts With Parkinson Disease
by Gutti, U., Fung, H.-C., Hruska, K. S., LaMarca, M. E., Chen, C.-M., Wu, Y.-R., Sidransky, E.


CORRESPONDENCE: The Need for Appropriate Genotyping Strategies for Glucocerebrosidase Mutations in Cohorts With Parkinson Disease--Reply
by Tan, E.-K.


CLINICAL TRIALS: Tesofensine (NS 2330), a Monoamine Reuptake Inhibitor, in Patients With Advanced Parkinson Disease and Motor Fluctuations: The ADVANS Study
by Rascol, O., Poewe, W., Lees, A., Aristin, M., Salin, L., Juhel, N., Waldhauser, L., Schindler, T., for the ADVANS Study Group


ORIGINAL CONTRIBUTION: Improvement in Parkinson Disease by Subthalamic Nucleus Stimulation Based on Electrode Placement: Effects of Reimplantation
by Anheim, M., Batir, A., Fraix, V., Silem, M., Chabardes, S., Seigneuret, E., Krack, P., Benabid, A.-L., Pollak, P.



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Journal of Neurology

Neuroleptic-induced parkinsonism is associated with olfactory dysfunction


Reply: Heart valve abnormalities in Parkinson’s disease treated with dopamine agonists


Heart valve abnormalities in Parkinson’s disease treated with dopamine agonists



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If you don’t see a long list of publications click on the title to show the latest publications.

Latest publications from Multiple Sclerosis journal, Journal of Neuroimmunnology and multiple sclerosis articles from general neurology journals. Subscribe to this list by clicking the orange RSS feed button: Subscribe to MS updates here.

Multiple Sclerosis

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[Research papers] Bone-marrow transplantation fails to halt intrathecal lymphocyte activation in multiple sclerosis
by Mondria, T, Lamers, C H J, Boekhorst, P A W t., Gratama, J W, Hintzen, R Q


[Research papers] Survival and cause of death in multiple sclerosis: a prospective population-based study
by Hirst, C, Swingler, R, Compston, D A S, Ben-Shlomo, Y, Robertson, N P


[Research papers] Characterisation of the spectrum of demyelinating disease in Western Australia
by Wu, J-S, Zhang, M-N, Carroll, W M, Kermode, A G


[Research papers] Effects of fluoxetine on disease activity in relapsing multiple sclerosis: a double-blind, placebo-controlled, exploratory study
by Mostert, J P, Admiraal-Behloul, F, Hoogduin, J M, Luyendijk, J, Heersema, D J, van Buchem, M A, De Keyser, J


[Research papers] Relapsing demyelinating disease affecting both the central and peripheral nervous systems
by Zephir, H, Stojkovic, T, Latour, P, Lacour, A, de Seze, J, Outteryck, O, Maurage, C-A, Monpeurt, C, Chatelet, P, Ovelacq, E, Vermersch, P



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Annals of Neurology

Will Rogers phenomenon in multiple sclerosis
by Maria Pia Sormani, Mar Tintorè, Marco Rovaris, Alex Rovira, Xavier Vidal, Paolo Bruzzi, Massimo Filippi, Xavier Montalban


Gray matter atrophy in multiple sclerosis: A longitudinal study
by Elizabeth Fisher, Jar-Chi Lee, Kunio Nakamura, Richard A. Rudick


Gray matter atrophy is related to long-term disability in multiple sclerosis
by Leonora K. Fisniku, Declan T. Chard, Jonathan S. Jackson, Valerie M. Anderson, Daniel R. Altmann, Katherine A. Miszkiel, Alan J. Thompson, David H. Miller


Alteration of cystatin C in the cerebrospinal fluid of multiple sclerosis
by Ichiro Nakashima, Kazuo Fujihara, Masakatsu Fujinoki, Takeshi Kawamura, Toshihide Nishimura, Masashi Nakamura, Yasuto Itoyama



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Neurology

Assessment: The use of natalizumab (Tysabri) for the treatment of multiple sclerosis (an evidence-based review): Report of the Therapeutics and Technology Assessment Subcom...
by Goodin, D. S., Cohen, B. A., O'Connor, P., Kappos, L., Stevens, J. C.



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Lancet Neurology

[Reflection and Reaction] Neutralisation of IL12 p40 or IL23 p40 does not block inflammation in multiple sclerosis
by Roland Martin


[Reflection and Reaction] B cells, antibodies, and tertiary lymphoid tissue in MS brains
by Olaf Stüve, Todd N Eagar


[Articles] Repeated subcutaneous injections of IL12/23 p40 neutralising antibody, ustekinumab, in patients with relapsing-remitting multiple sclerosis: a phase II, double-b...
by Benjamin M Segal, Cris S Constantinescu, Aparna Raychaudhuri, Lilianne Kim, Rosanne Fidelus-Gort, Lloyd H Kasper, on behalf of the Ustekinumab MS Investigators


[Review] Grey matter pathology in multiple sclerosis
by Jeroen JG Geurts, Frederik Barkhof


[Personal View] B cells and multiple sclerosis
by Diego Franciotta, Marco Salvetti, Francesco Lolli, Barbara Serafini, Francesca Aloisi



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Brain

Perivascular spaces--MRI marker of inflammatory activity in the brain?
by Wuerfel, J., Haertle, M., Waiczies, H., Tysiak, E., Bechmann, I., Wernecke, K. D., Zipp, F., Paul, F.


Gadofluorine M enhancement allows more sensitive detection of inflammatory CNS lesions than T2-w imaging: a quantitative MRI study
by Bendszus, M., Ladewig, G., Jestaedt, L., Misselwitz, B., Solymosi, L., Toyka, K., Stoll, G.


Naive CD8 T-cells initiate spontaneous autoimmunity to a sequestered model antigen of the central nervous system
by Na, S.-Y., Cao, Y., Toben, C., Nitschke, L., Stadelmann, C., Gold, R., Schimpl, A., Hunig, T.


Neurogenesis in the chronic lesions of multiple sclerosis
by Chang, A., Smith, M. C., Yin, X., Fox, R. J., Staugaitis, S. M., Trapp, B. D.


Mutation of FIG4 causes a rapidly progressive, asymmetric neuronal degeneration
by Zhang, X., Chow, C. Y., Sahenk, Z., Shy, M. E., Meisler, M. H., Li, J.


Do natural killer cells accelerate or prevent autoimmunity in multiple sclerosis?
by Lunemann, J. D., Munz, C.


From fish to man: understanding endogenous remyelination in central nervous system demyelinating diseases
by Dubois-Dalcq, M., Williams, A., Stadelmann, C., Stankoff, B., Zalc, B., Lubetzki, C.


Cytometric profiling in multiple sclerosis uncovers patient population structure and a reduction of CD8low cells
by De Jager, P. L., Rossin, E., Pyne, S., Tamayo, P., Ottoboni, L., Viglietta, V., Weiner, M., Soler, D., Izmailova, E., Faron-Yowe, L., O'Brien, C., Freeman, S., Granados, S., Parker, A., Roubenoff, R., Mesirov, J. P., Khoury, S. J., Hafler, D. A., Weiner, H. L.


Strong EBV-specific CD8+ T-cell response in patients with early multiple sclerosis
by Jilek, S., Schluep, M., Meylan, P., Vingerhoets, F., Guignard, L., Monney, A., Kleeberg, J., Le Goff, G., Pantaleo, G., Du Pasquier, R. A.


Mitochondrial defects in acute multiple sclerosis lesions
by Mahad, D., Ziabreva, I., Lassmann, H., Turnbull, D.


Abnormally phosphorylated tau is associated with neuronal and axonal loss in experimental autoimmune encephalomyelitis and multiple sclerosis
by Anderson, J. M., Hampton, D. W., Patani, R., Pryce, G., Crowther, R. A., Reynolds, R., Franklin, R. J. M., Giovannoni, G., Compston, D. A. S., Baker, D., Spillantini, M. G., Chandran, S.


Differentiation block of oligodendroglial progenitor cells as a cause for remyelination failure in chronic multiple sclerosis
by Kuhlmann, T., Miron, V., Cuo, Q., Wegner, C., Antel, J., Bruck, W.


Clinical and radiographic spectrum of pathologically confirmed tumefactive multiple sclerosis
by Lucchinetti, C. F., Gavrilova, R. H., Metz, I., Parisi, J. E., Scheithauer, B. W., Weigand, S., Thomsen, K., Mandrekar, J., Altintas, A., Erickson, B. J., Konig, F., Giannini, C., Lassmann, H., Linbo, L., Pittock, S. J., Bruck, W.


Non-communicating syringomyelia: a feature of spinal cord involvement in multiple sclerosis
by Weier, K., Naegelin, Y., Thoeni, A., Hirsch, J. G., Kappos, L., Steinbrich, W., Radue, E.-W., Gass, A.


Intra-cortical connectivity in multiple sclerosis: a neurophysiological approach
by Tecchio, F., Zito, G., Zappasodi, F., Dell' Acqua, M. L., Landi, D., Nardo, D., Lupoi, D., Rossini, P. M., Filippi, M. M.



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Archives of Neurology

ORIGINAL CONTRIBUTION: Reduction of Disease Activity and Disability With High-Dose Cyclophosphamide in Patients With Aggressive Multiple Sclerosis
by Krishnan, C., Kaplin, A. I., Brodsky, R. A., Drachman, D. B., Jones, R. J., Pham, D. L., Richert, N. D., Pardo, C. A., Yousem, D. M., Hammond, E., Quigg, M., Trecker, C., McArthur, J. C., Nath, A., Greenberg, B. M., Calabresi, P. A., Kerr, D. A.


OBSERVATION: Clinical and Neuropathologic Findings in a Woman With the FMR1 Premutation and Multiple Sclerosis
by Greco, C. M., Tassone, F., Garcia-Arocena, D., Tartaglia, N., Coffey, S. M., Vartanian, T. K., Brunberg, J. A., Hagerman, P. J., Hagerman, R. J.


ORIGINAL CONTRIBUTION: Retinal Imaging by Laser Polarimetry and Optical Coherence Tomography Evidence of Axonal Degeneration in Multiple Sclerosis
by Zaveri, M. S., Conger, A., Salter, A., Frohman, T. C., Galetta, S. L., Markowitz, C. E., Jacobs, D. A., Cutter, G. R., Ying, G.-S., Maguire, M. G., Calabresi, P. A., Balcer, L. J., Frohman, E. M.


OBSERVATION: Lewis-Sumner Syndrome and Tangier Disease
by Theaudin, M., Couvert, P., Fournier, E., Bouige, D., Bruckert, E., Perrotte, P., Vaschalde, Y., Maisonobe, T., Bonnefont-Rousselot, D., Carrie, A., Le Forestier, N.


BOOK REVIEWS: The Clinical Neuropsychiatry of Multiple Sclerosis, 2nd Edition
by Brousseau, K.


ORIGINAL CONTRIBUTION: Multiple Sclerosis Risk After Optic Neuritis: Final Optic Neuritis Treatment Trial Follow-up
by The Optic Neuritis Study Group


ORIGINAL CONTRIBUTION: Neuroprotection and Immunomodulation With Mesenchymal Stem Cells in Chronic Experimental Autoimmune Encephalomyelitis
by Kassis, I., Grigoriadis, N., Gowda-Kurkalli, B., Mizrachi-Kol, R., Ben-Hur, T., Slavin, S., Abramsky, O., Karussis, D.


OBSERVATION: Vitamin D-Dependent Rickets as a Possible Risk Factor for Multiple Sclerosis
by Torkildsen, O., Knappskog, P. M., Nyland, H. I., Myhr, K.-M.


OBSERVATION: Seven-Tesla Magnetic Resonance Imaging: New Vision of Microvascular Abnormalities in Multiple Sclerosis
by Ge, Y., Zohrabian, V. M., Grossman, R. I.


OBSERVATION: Progressive Supranuclear Palsy With Walleyed Bilateral Internuclear Ophthalmoplegia Syndrome
by Matsumoto, H., Ohminami, S., Goto, J., Tsuji, S.


ORIGINAL CONTRIBUTION: Increased Osteopontin Levels in the Cerebrospinal Fluid of Patients With Multiple Sclerosis
by Braitch, M., Nunan, R., Niepel, G., Edwards, L. J., Constantinescu, C. S.


OBSERVATION: Allergic and Nonallergic Delayed Infusion Reactions During Natalizumab Therapy
by Hellwig, K., Schimrigk, S., Fischer, M., Haghikia, A., Muller, T., Chan, A., Gold, R.


RESEARCH LETTERS: Atorvastatin Does Not Alter Interferon Beta-Induced Changes of Serum Matrix Metalloproteinase 9 and Tissue Inhibitor of Metalloproteinase 1 in Patients Wi...
by Sellner, J., Greeve, I., Leib, S. L., Mattle, H. P.


CORRESPONDENCE: Multiple Sclerosis and Recurrent Disseminated Encephalomyelitis Are Different Diseases
by Poser, C. M.


CORRESPONDENCE: Multiple Sclerosis and Recurrent Disseminated Encephalomyelitis Are Different Diseases--Reply
by de Seze, J.


CORRESPONDENCE: Monophasic Acute, Recurrent, and Multiphasic Disseminated Encephalomyelitis and Multiple Sclerosis
by Brinar, V. V., Habek, M.


CORRESPONDENCE: Monophasic Acute, Recurrent, and Multiphasic Disseminated Encephalomyelitis and Multiple Sclerosis--Reply
by de Seze, J.


CORRESPONDENCE: Differential Diagnosis Between Acute Disseminated Encephalomyelitis and Multiple Sclerosis During the First Episode
by Tavazzi, E., Ravaglia, S., Franciotta, D., Marchioni, E.


CORRESPONDENCE: Differential Diagnosis Between Acute Disseminated Encephalomyelitis and Multiple Sclerosis During the First Episode--Reply
by de Seze, J.



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Journal of Neurology

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Latest Epilepsy publications from Epilepsia and filtered articles from the General Neurology Journals (Seizure will be added once they upgrade to using RSS technology!):

>Subscribe to Epilepsy updates here

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[Research papers] Effects of albendazole treatment on neurocysticercosis: a randomised controlled trial
by Carpio, A, Kelvin, E A, Bagiella, E, Leslie, D, Leon, P, Andrews, H, Hauser, W A, the Ecuadorian Neurocysticercosis Group



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This includes latest publications from AHA Stroke Journal and filtered articles from general neurology journals on stroke:

AHA Stroke Journal: “Stroke”

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Journal of Neurology, Neurosurgery and Psychiatry

[Research papers] Risk profiles for mild cognitive impairment and progression to dementia are gender specific
by Artero, S, Ancelin, M-L, Portet, F, Dupuy, A, Berr, C, Dartigues, J-F, Tzourio, C, Rouaud, O, Poncet, M, Pasquier, F, Auriacombe, S, Touchon, J, Ritchie, K


[Research papers] Depressive symptoms and risk of stroke: the Rotterdam Study
by Bos, M J, Linden, T, Koudstaal, P J, Hofman, A, Skoog, I, Breteler, M M B, Tiemeier, H


[Research papers] Cerebral microbleeds in the population based AGES-Reykjavik study: prevalence and location
by Sveinbjornsdottir, S, Sigurdsson, S, Aspelund, T, Kjartansson, O, Eiriksdottir, G, Valtysdottir, B, Lopez, O L, van Buchem, M A, Jonsson, P V, Gudnason, V, Launer, L J


[Short reports] Utility of the stroke-thrombolytic predictive instrument
by Uyttenboogaart, M, Stewart, R E, Vroomen, P C, Luijckx, G-J, De Keyser, J



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Annals of Neurology

Takotsubo cardiomyopathy in acute ischemic stroke
by Sohei Yoshimura, Kazunori Toyoda, Tomoyuki Ohara, Hikaru Nagasawa, Noriko Ohtani, Takahiro Kuwashiro, Hiroaki Naritomi, Kazuo Minematsu


Admission international normalized ratio and acute infarct volume in ischemic stroke
by Hakan Ay, Ethem Murat Arsava, Levent Gungor, David Greer, Aneesh B. Singhal, Karen L. Furie, Walter J. Koroshetz, A. Gregory Sorensen


Motor outcome prediction using diffusion tensor tractography in pontine infarct
by Sung Ho Jang, Daiseg Bai, Su Min Son, Jun Lee, Dae-Shik Kim, Joon Sakong, Dong Gyu Kim, Dong Seok Yang


Calcification and endothelialization of thrombi in acute stroke
by Mohammed A. Almekhlafi, William Y. Hu, Michael D. Hill, Roland N. Auer



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Neurology

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Lancet neurology

[Reflection and Reaction] “Telethrombolysis”: stroke consultation by telemedicine
by Pierre Amarenco


[Reflection and Reaction] Lancet Asia Medical Forum—call for papers
by Helen Frankish


[Articles] Efficacy of site-independent telemedicine in the STRokE DOC trial: a randomised, blinded, prospective study
by Brett C Meyer, Rema Raman, Thomas Hemmen, Richard Obler, Justin A Zivin, Ramesh Rao, Ronald G Thomas, Patrick D Lyden



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Brain

Lateropulsion, pushing and verticality perception in hemisphere stroke: a causal relationship?
by Perennou, D. A., Mazibrada, G., Chauvineau, V., Greenwood, R., Rothwell, J., Gresty, M. A., Bronstein, A. M.


Soluble amyloid-{beta} peptides potently disrupt hippocampal synaptic plasticity in the absence of cerebrovascular dysfunction in vivo
by Hu, N.-W., Smith, I. M., Walsh, D. M., Rowan, M. J.


1H/13C MR spectroscopic imaging of regionally specific metabolic alterations after experimental stroke
by van der Zijden, J. P., van Eijsden, P., de Graaf, R. A., Dijkhuizen, R. M.


Mitochondrial defects in acute multiple sclerosis lesions
by Mahad, D., Ziabreva, I., Lassmann, H., Turnbull, D.



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Archives of Neurology

ORIGINAL CONTRIBUTION: Anticoagulation After Cardioembolic Stroke: To Bridge or Not to Bridge?
by Hallevi, H., Albright, K. C., Martin-Schild, S., Barreto, A. D., Savitz, S. I., Escobar, M. A., Gonzales, N. R., Noser, E. A., Illoh, K., Grotta, J. C.


NEUROLOGICAL REVIEW: Percutaneous Clot Removal Devices in Acute Ischemic Stroke: A Systematic Review and Meta-analysis
by Stead, L. G., Gilmore, R. M., Bellolio, M. F., Rabinstein, A. A., Decker, W. W.


ORIGINAL CONTRIBUTION: Thrombolysis in Patients With Marked Clinical Fluctuations in Neurologic Status Due to Cerebral Ischemia
by Ozdemir, O., Beletsky, V., Chan, R., Hachinski, V.


IMAGES IN NEUROLOGY: Golfer's Stroke From Internal Carotid Artery Dissection
by Choi, K.-D., Oh, S.-J., Yang, T.-i., Lee, T.-H.


BOOK REVIEWS: Management of Stroke: A Practical Guide for the Prevention, Evaluation, and Treatment of Acute Stroke, 3rd ed
by Ohanian, A. G., Liebeskind, D. S.


NEUROLOGICAL REVIEW: Rural-Urban Differences in Acute Stroke Management Practices: A Modifiable Disparity
by Leira, E. C., Hess, D. C., Torner, J. C., Adams, H. P.