The posterior inferior cerebellar artery also known as PICA is the largest branch of the vertebral artery, passes on an irregular course between Medulla and Cerebellum.  It is one of the 3 major arteries supplying  the cerebellum. It supplies the posterior part of inferior surface of Vermis, Central nucleii of Cerebellum and undersurface of Cerebellar hemisphere.It also supplies  Medulla ( branches of PICA along with medullary branches of Vertebral artery) and Choroid Plexus of 4 th ventricle.

Adolf Wallenberg (November 10, 1862-1949) ,a German internist and neurologist, first described the clinical manifestations (1895) and the autopsy findings (1901) in occlusions of the arteria cerebelli posterior inferior (Wallenberg syndrome)

Cause :-

• It results from thrombosis of Posterior Inferior Cerebellar Artery.
• Causing lateral part of the medulla oblongata to infarct.
• The most commonly affected artery is the vertebral artery, followed by the PICA, superior middle and inferior medullary arteries.

Lateral Medullary syndrome of Wallenberg

Signs and Symptoms that are Characteristic of Wallenberg Syndrome are-

1. Dysphagia and Dysarthria ( Due to paralysis of Ipsilateral palatal and laryngeal muscles- Innervated by Nucleus Ambiguus)
2. Analgesia and Thermaesthesia on the Ispsilateral side of the face ( Due to lesion of Nucleus and Spinal tract of Trigeminal nerve)
3. Vertigo, Nausea, Vomiting and Nystagmus. ( Lesion of Vestibular nucleii)
4. Ipsilateral Horner Syndrome ( due to lesion of Descending Sympathetic fibres)   Mnemonic- “Horny PAMELa” for Ptosis, Anhydrosis, Miosis, Enophthalmos and Loss of ciliospinal reflex
5. Cerebellar Symptoms and Signs-

• • Cerebellar Ataxic/ Drunken Gait
  • Dysdiadochokinesia ( unable to perform quick alternative repeated actions like pronation/supination)
  • Pendular knee jerk
  • Nystagmus
  • Dysmetria
  • Intention Tremor ( Tremor increases as fingers arrive the target)
  • Hypotonia
  • Rebound phenomenon
  • Scanning speech

In Lateral Medullary Syndrome  following structures are affected-

1. Nucleus Ambiguus
2. Nucleus Solitarius
3. Vestibular Nucleus
4. Cochlear Nucleus
5. Spinocerebellar tracts
6. Lateral Spinothalmic tract
7. Spinal Nucleus of  Trigeminal Nerve
8. Tract of  Trigeminal Nerve

“The Only way not to miss the Diagnosis is to keep PICA syndrome in mind, then you can head for confirmation”

Introduction:

Migraine is the 2^nd most common cause of headache affecting 15% of women and 6 % of men worldwide. It is an episodic headache associated with certain features like sensitivity to light light, sound or movement . Nausea vomiting often accompany the headache.

Triggers for Migraine Headache:

Hormonal Changes:- Changes during menses, pregnancy, menopause, and effect of OCP
Changes in daily schedule:- over sleeping, inadequate sleep, skipping meal and a rest after a hectic schedule.
Weather:- Rapidly rising barometric pressure, rise in pressure, temperature and humidity
Foods:- food rich in tyramin like aged cheese, chocolate,banana, soya sauce and citrus fruits
Environmental triggers like cigarette smoke, perfumes, petrol and fresh paint

Migraine Headache

Pathogenesis of Migraine ( PDF format)

Variants Of Migraine:

1. Hemiplegic migraine-  weakness which is usually reversible
2. Basilar Migraine- dizziness,ataxia,tinnitus, vomiting
3. Retinal Migraine- recurrent attack of unilateral visual disturbances
4. Complicated Migraine- chronic migraine and status migraines.
5. Ophthalmoplegic Migraine- Associated with periorbital pain, diplopia sec to cranial neuropathies.

Symptoms:-

• Nausea
• Lightheadedness
• Vomiting
• Vertigo
• Seizure
• Diarrhoea
• Photophobia
• Scalp tenderness
• Visual disturbances
• Syncope
• Confusion

Diagnosis:

Diagnosis is Clinical, No investigations are mandatory.

Diagnostic Criteria for Migraine:-

Repeated attacks of Headache lasting 4-72 hours in patient with normal physical examination and no other reasonable cause for headache, and

Atleast 2 of the following features:

• Unilateral pain
• Throbbing pain
• Aggravated by movements
• Moderate to severe intensity

Plus Atleast 1 of the following features:

• Nausea/ Vomiting
• Photophobia or Phonophobia

Management Of Migraine Headache:-

MIDAS ( Migraine Disability Assessment Score) is a well validated tool , on the basis of which Migraine is Graded from I to IV

General Measures Against Migraine:

1. Identify and Avoid Trigger factors
2. Regular exercise and healthy diet
3. Regular sleep pattern, avoid alcohol
4. Yoga .

Medical Management:

Judicious use of 1 or more drug is the mainstay of treatment:

• Mild cases- Oral agents
• Sever cases- Parental therapy

1. NSAIDS- decrease both severity + Duration. Naproxen, Ibuprofen are good enough
2. 5 HT1 agonists- Sumatriptan, Naratriptan,
3. Parental Inj Dihydroergotamine + Sumatriptan is FDA approved therapy
4. Dopamine Antagonists:- Metoclopramide, Prochlorperazine are used as adjunctive therapy

Other Agents are:

1. Nasal BUTHORPHANOL
2. Oral Acetaminophen + Dichloralphenazone+ Isomethaptene
3. Parental Meperidine ( 50-100 mg )

Prophylaxis therapy In Migraine headache:

According to the British Assocaiation for Study of Headache, Prophylaxis are required when any of:-

1. Frequent disabling attacks > 2 per month inspite of Acute therapy
2. Failure of acute Therapy
3. Hemiplegic migraine, Basilar Migraine
4. Very high attack frequency( >2/week)
5. Progressively worsening attack.
6. Patients Request

Calcium Channel Blocker – FLUNARIZINE  5-10 mg reduces the frequency by 50-75%. Women require lower doses.

NSAIDS- NAPROXEN
Beta Blockers- PROPONALOL
TCA
Botulinum Toxin

Read about http://www.merckmedicus.com/pp/us/hcp/diseasemodules/migraine/pathophysiology_sub.jsp

Simplified: http://www.mayoclinic.com/health/migraine-headache/DS00120

SOURCE: Lecture notes from Harrison, Davidson and ache.org

Anatomic Basis:
Amygdala lies deep within medial temporal lobes of the brain. The centromedial amygdala projects through the stria terminalis primarily to the hypothalamus and through the ventral amygdalofugal tract to the brain stem, where it can influence hormonal and somatomotor aspects of behavior & emotional states (eating, drinking & sex).

Monkey Experiment:

Heinrich Kluver and Paul Bucy found that the bilateral removal of the temporal lobe in rhesus monkeys caused a dramatic effect on the animal’s behavior. The set of behavioral changes were:

1. Visual agnosia (psychic blindness): Inability to recognize or interpret objects in the visual field
2. Increased oral tendency (hyperorality): Tendency to place everything in mouth and sometimes even tries to eat solid objects
3. Hypermetamorphosis: Extreme curiosity about everything
4. Decreased emotional reactions: Dulled emotions and Less expressive facial movements and vocalisations. They lost fear where it would normally occur. Even after being attacked by a snake, they would casually approach it again. This was called “placidity”.
5. Increased sexual behavior: Sex drive so strong that it attempts to copulate with immature animals, animals of the wrong sex or even animals of different species
6. Forgets rapidly
7. Reduced maternal behavior: Monkey mothers showed a reduction in maternal behaviors towards their infants, often physically abusing or neglecting them

Signs and Symptoms:

1. Inability to recognize people
2. Lack of fear reaction and rage reaction
3. Emotional flatenning (placidity)
4. Short term memory loss
5. Hypersexuality (lack social sexual restraint)
6. Hyperphagia
7. Bulimia
8. Weight gain (Read about complications of obesity)
9. Socially inappropriate licking or touching
10. Seizures

Causes:

1. Facial or cerebral trauma
2. Temporal lobectomy
3. Herpes Simplex encephalitis
4. Meningoencephalitis
5. Niemann Pick disease of the brain
6. Alzheimer’s disease
7. Progressive subcortical gliosis
8. Rett syndrome
9. Porphyria (Read about Porphyria: A true story of Vampire)
10. Carbon monoxide poisoning
11. Cerebrovascular disease
12. Hypoglycemia

Diagnosis:

1. Neuroimaging
2. Frontotemporal dementia
3. MRI (Magnetic Resonance Imaging)
4. SPECT (Single Photon Emission Computed Tomography)

Treatment:
The disease is incurable but symptomatic treatment may include drug therapy.

Case Report:

1. Case of a 43 year old man who developed features of Kluver-Bucy Syndrome
2. Case of a 24 year old Korean women who met with motor vehicle accident

“ Akinetic Rigid Syndrome’ or Idiopathic Parkinson Disease-Are a number of degenerative diseases affecting Basal Ganglia which present with differing combinations of

• Bradykinesia
• Rigidity
• Tremor
• Loss of postural reflex

Epidemiology-

• 90% cases are above 45 years
• Male  and Female have equal risk
• Cigarette smoking is known to be protective.

Cause or Etiology-

• Unknown but toxin called MPTP ( Methyl-Phenyl-Tetrahydropyridine) suspected if disease starts in Young.

Pathology-

Symptoms are the result of depletion of Pigmented Dopaminergic neurons in Substancia Nigra causing impairment in dopaminergic transmission through the NigroStriatal pathway. Lewy Bodies are seen in Nigral cells. Atrophic changes in S. nigra and decrease neurons in Locus Cerulous.

Clinical Features-

source: Brainmind.com

Initial symptoms include- Tiredness, Aching limbs, Mental slowness, Depression and Micrographia ( small handwriting)

General features-

• Expressionless face ( Hypomimia)
• Greasy skin
• Soft Rapid indistinct speech
• Flexed posture
• Impaired postural reflexes

Gait- Festinate Gait is typical of Parkinsonism.  Slow to start walking, short strides, reduced arm swing and loss of balance on turning can occur.

Tremors-

• Resting tremor is typical for Parkinsonism. Coarse tremors usually thumb and fingers ‘ Pill Rolling motion’ , later whole body may have tremors.
• Postural tremors are less obviously noticed but are present

Rigidity-

• Cog Wheel Rigidity- Rigidity with Tremor. Movement become like turning of Cog-wheel .
• Lead Pipe or Plastic Rigidity

Bradykinesia -

• Slowness in Initiating and repeating movements
• Poor fine-movements

Investigations-

Diagnosis is made Clinically

CT, MRI to rule out other causes of tremor like Wilsons Disease.

Management:

LevoDopa ( Dopamine Precursor) + Carbidopa / Benserazide ( Peripheral Dopa Decarboxylase Inhibitor) Is Best combination for treatment of Parkinsonism.

Others- Trihexiphenidyl ( Benzhexol) Or Orphenadrine help to cope with Cholinergic Side-effects of above drugs.

Amantadine ( anti-flu drug) has no effect on Bradykinesia but worksfor Rigidity and Tremor

Entacapone- ( COMT Inhibitor)

Selegiline ( MAO-B Inhibitor)

Dopamine Receptor Agonists like – Apomorphine, Domperidome, Bromocriptine, Pergolide, Ropinirole and Pramipexole are sometimes used.

Surgery-

• Sterotactic Thalamotomy
• Pallidotomy
• Implantation Of fetal midbrain cells in basal ganglia is under experiment.

Speech Therapy and Physiotherapy

Warning- Do not take drug without Physicians Prescription.

Source- Davidson’s Medicine, Lecture Notes.

Details Reading and latest researches on PD – Interested readers http://en.wikipedia.org/wiki/Parkinson’s_disease