Head in the Clouds

Approach to the Headache:

Primary vs Secondary, and Intracranial vs Extracranial:

Intracranial–Pain sensitive structures in the brain includes venous sinuses, cortical veins, basal arteries, dura of anterior, middle, and posterior fossae.

Extracranial—Scalp vessels and muscles, orbital contents, mucous membranes of nasal and paranasal spaces, external and middle ear, teeth, and gums.

Primary Headaches:          

  1. Tension: Most common, diffuse, dull, band-like headache, worse when touching scalp. May become worse towards the end of the day, aggravated by noise. Mechanism: muscular due to contraction of jaw, teeth, brow. Tx: Amitriptyline and tricyclic antidepressants or β blockers.

2. Migraine: Unilateral throbbing headache, onset in childhood or early adult life. Affects 5-10% of population, with female predominance and has family history. With or without aura (flashing lights, zigzags, scintillating scotoma, visual field defects), worsened by bright light, relieved by sleep, associated with nausea and occasionally vomiting. Some types of migraine (Basilar, Hemiplegic, retinal) may be associated with severe symptoms such as tetraparesis or hemiparesis, unsteadiness, dysarthria, vertigo, bilateral visual symptoms.

May go through phases: Premonition or prodromalà Aura à Headache àResolution.

Precipitating factors:

Diatary: alcohol, chocolate, cheese (contains tyramine)

Hormonal: Premenstrual or oral contraceptive (fluctuating oestrogen)

Stress, physical fatigue, exercise, sleep deprivation and minor head trauma.

D/D with: Partial epilepsy, transient ischemic attack, arteriovenous malformation, hypoglycemia.

Tx: Analgesics, sumatriptan, ergotamine, prophylaxis (5HT2 receptor blocker Pizotifen, or propranolol (beta adrenergic receptor blocker)), calcium antagonists (verapamil), antipressants (amitriptyline), anticonvulsants (topiramate or sodium valproate).

  1. Cluster: (Histamine cephalgia, migrainous neuralgia) Often in men in middle age, severe unilateral pain lasting 10 mins to 2 hours around the eye, associated with conjunctival injection, lacrimation, rhinorrhea, and transient Horner’s (miosis, ptosis, anhidrosis). Alcohol may precipitate. 

Secondary Headaches:

  1. Sinus headache
  2. Medication overuse
  3. Meningitis and other infections
  4. Post-traumatic
  5. Intracranial hypotension
  6. Increased intracranial hypertension
  7. Brain tumor or aneurysm
  8. Cervicogenic headache
  9. Temporal arteritis
  10. Acute close angle glaucoma

Differentiate using the SNOOP list:

  1. Systemic Signs or Symptoms: Look for the presence of fever, weight loss, history of cancer, abnormal blood tests; this could point to meningitis, cancer, or illness to be the cause of the headache.
  2. Neurologic Exam: if the neurologic exam is abnormal, then consider secondary headache as the cause. Eg: abnormal speech, gait, confusion, and dizziness.
  3. Onset: Sudden, abrupt, or split-second.
  4. Onset: if less than age 5 or new onset greater than 50 years old
  5. Progressive: this would refer to a headache pattern that is progressively worsening over time. (Or previous headache history).

Reassuring history of a primary headache:

  1. Stable pattern of headache for over 6 months
  2. Predictable triggers for a headache
  3. Individual feels fine between attack

2. Assessment of upper extremities:

Observe: For muscle wasting, fasciculations, asymmetry, or walkers and other assistant devices beside the bed.

Tone and Clonus:

Tone may be increased due to UMN lesion (Spasticity), or due to extrapyramidal tract (Rigidity). It can also decrease due to LMN lesions (Flaccidity). Tested by supporting elbow and shaking hand, then rapidly supinate and pronate arm. Test spasticity by flexion of elbow and watch for cogwheel or clasp knife.

Limb Power:

Abduct arm >90 degrees; Deltoid   ; Axillary n.;   C5-6

Elbow flexion: Biceps, brachialis;   Musculocut. n.;   C5-6

Wrist flexion: Flexor carpi radialis; median n.; C6-7

Finger Flexion: Flexor digitorum profundus; ulnar n.; C7-8

Finger extension: Extensor digitorum or extensor digiti minimi; Radial n.; C7-8

Wrist extension: Extensor carpi radialis, Radial n.; C7-8

Elbow extension: Triceps; Radial nerve; C7-8

Finger ADDUCTION: Adductor policis, Ulnar n.; V8, T1

Finger ABDUCTION: Abductor pollicis brevis; median n.; C8, T1

Thumb up: Abductor pollicis longus + brevis, Ulnar nerve, C8, T1

3. Assessment of Lower Extremities:

Tone: Logroll, flex and extend the knee.

Rapid dorsiflexion: ankle clonus

Limb power:

Hip flexion: ilio-psoas; Femoral n.; L2-3

Knee extension: Quadraceps; Femoral n.; L3-4

Foot dorsiflexion: Tibialis anterior; Deep peroneal n.; L4-5

Foot plantarflexion: Gastrocnemius, Soleus; Tibial n.; S1-2

Knee Flexion: Hamstrings; Sciatic n.; L5-S1

Hip Extension: Gluteus max; Inferior gluteal n,; L5-S1,2

Hip Adduction: Adductors; Obturator n.; L2-3-4

Hip abduction: Gluteus med + Min+ tensor fascia latae; Sup. Gluteal n,; L4-5 S1

Eversion: Peroneus longus + brevis; Superficial peroneal n.; L5-S1

Inversion: Tibialis posterior; Tibial n.; L5-S1

Toe extension: Ext. hallucis longus, ext. digitorum longus; Deep peroneal n.; L4-5

4. Descending Tracts:

Pyramidal tracts:

Corticospinal tracts:

  1. Start from primary motor, premotor, and supplementary motor, as well as somatosensory area
  2. Descends through internal capsule
  3. Through crus cerebri of midbrain, to pons and medulla
  4. Divides into Lateral and Anterior tracts
  5. Anterior corticospinal tract remains ipsilateral
  6. Lateral corticospinal tract descends contralaterally to ventral horn and to lower motor neuron.

Corticobulbar tracts:

  1. Primary motor cortex (lateral)
  2. Brain stem
  3. Cranial nerves
  4. Face and neck (Bilateral innervation except 7 and 12)

Extrapyramidal Tracts:

  1. Vestibulospinal Tracts: Vestibular nuclei, receives input from organs of balance, controls ipsilateral balance and posture, anti-gravity muscles.
  2. Reticulospinal Tracts: Medial RST arise from pons, facilitates voluntary movements and increase muscle tone, lateral RST arises from medulla, and inhibits voluntary movements, and reduce muscle tone.
  3. Rubrospinal Tracts: Originates from red nucleus in midbrain, they decussate and descend with contralateral innervation, plays a role in fine control of hand movements.
  4. Tectospinal Tracts: Begins at superior colliculus of midbrain, receives input from optic nerves, coordinates movements of the head in relation to visual stimuli.

5. Ascending Tracts:

Conscious Tracts:

  1. Dorsal column medial lemniscus pathway:

DCML: Sensory, tactile (fine touch), vibration, proprioception.

1o Upper limb signals (T6 and above)- Fascicus cuneatus (lateral), synapse at nucleus cuneatus of the medulla oblongata. (Lower limb signals below T6 go in the fasciculus gracilis (medial), and synapse at nucleus gracillis)

2o Cuneate or gracilis nucleus dicussate at medulla, travel in the contralateral medial lemniscus and reach the Ventral posterolateral nucleus of thalamus.

3o At VPL nucleus it goes through internal capsule to sensory cortex.

  1. Anterolateral system (Spinothalamic tract):

Lateral spinothalamic tract (Pain and temperature)

Anterior spinothalamic tract (touch and pressure)

1o Skin to dorsal spinal cord, ascend 1 or 2 levels via Lissauer’s tract, to synapse at tip of dorsal horn called Substantia Gelatinosa.

2o Substantia gelatinosa: Decussates at anterior white commissure and goes to VPL nucleus of thalamus.

3o From VPL nucleus to the sensory cortex.

Unconscious Tracts:  Spinocerebellar tracts:

  1. Posterior (lower limbs)
  2. Anterior (lower limbs)
  3. Rostral (Upper limbs)
  4. Cuneocerebellar (Upper limbs)
Advertisements
Head in the Clouds

Who’s Eyeing You?

Opthalmoplegia: weakness or paralysis of one or more extraocular muscles responsible for eye movements. Two types: internuclear vs external.

1. Causes of opthalmoplegia:
Internuclear: Traumatic, or neurological causes such as:

  • Multiple sclerosis: Demyelinating disorder, often affects bilaterally
  • Cranial nerves: Oculomotor, trochlear, abducens
  • Foville’s Syndrome: Brainstem stroke
  • Parinaud’s Syndrome: Dorsal midbrain
  • Frontal eye fields: Intersection of precentral and middle frontal gyrus.

External: Muscular or mitochondrial disorders such as:

  • Graves disease: Graves’ opthalmopathy associated with various signs.
  • Kearns-Sayre Syndrome: Mitochondrial disease characterized by  progressive external opthlamoplegia (PEO), pigmentary retinitis and onset before 20 years-old. Common additional S/S: Deafness, cerebellar ataxia, heart block.
  • Toxic envenomation: mambas, taipans, kraits
  • Thiamine deficiency: Wernicke’s encephalopathy
  • Lyme disease: Borrelia burgdorferi: causes not only uveitis, but also keratitis, iridocyclitis, vitritis, multifocal choroiditis, exudative retinal detachment and panophthalmitis.

2. Central lesions affecting horizontal gaze:

In order for both eyes to look at the same side, central lesions usually affect at least one of the following sites:

  1. Contralateral frontal eye field
  2. Ipsilateral PPRF
  3. Ipsilateral abducens nucleus
  4. Contralateral MLF
  5. Contralateral oculomotor nucleus

Note that the oculomotor nucleus is in the midbrain, and PPRF and abducens nucleus sits in the pons, with the abducens nucleus near the bottom. Also note MLF is not a nucleus but rather a fasciculus that connects not only the oculomotor and abducens, but also trochlear and vestibular nuclei.

pprf

pprf path

Pathway is as follows:  Say you want to make both eyes look LEFT. Signal starts from the RIGHT frontal eye field to the left PPRF, and goes to the left abducens nucleus. There the abducens nucleus sends a signal both to the lateral rectus of the left eye telling it to abduct and to the right oculomotor nucleus which causes the medial rectus of the right eye to adduct.

Lesion examples:

  1. Frontal eye field: contralateral bilateral gaze palsy
  2. PPRF and Abducens nucleus: Ipsilateral bilateral gaze palsy (PPRF: saccades, Abducens nucleus: saccades+VOR vestibule-ocular reflex)
  3. MLF (INO) : Contralateral gaze palsy with contralateral nystagmus.
  4. One and a Half Syndrome: One sided MLF and Abducens nucleus causes ipsilateral bilateral gaze palsy AND contralateral gaze palsy with contralateral nystagmus.
  5. Oculomotor opthalmoplegia: Ipsilateral adduction palsy.
  6. Foville’s Syndrome: (Posterior INO) Ipsilateral bilateral gaze palsy (conjugate gaze palsy, contralateral limb paralysis, and ipsilateral facial paralysis.
  7. WEBINO syndrome: Wall Eyed Bilateral INO: rostral lesion within the midbrain, may cause bilateral divergence.

ex

3. Central lesions affecting vertical gaze:

Upward vertical gaze palsy: Parinaud’s syndrome (Dorsal midbrain syndrome)

Lesion in the rostral midbrain (near oculomotor nucleus and pretectal area) (pineal tumors) causes paralysis of vertical gaze and failure of convergence, but retention of normal lateral gaze. Affects all vertical eye movements including saccades. Patient has: Sunset Eyes Sign, Collier Sign (bilateral lid retraction), large, irregular pupils that do not react to light but may react to near-far accommodation. Doll’s head maneuver should elevate the eyes, but eventually all upward gaze mechanisms fail.

Downward gaze palsies: progressive supranuclear palsy, lesions of rostral interstitial nucleus of the MLF (riMLF). Normally has bilateral effects on elevator muscles: superior rectus and inferior oblique muscles; as well as depressor muscles: inferior rectus and oblique muscles, thereore lesions to the riMLF has more effect on downward than upward saccades.

Bonus: Locked-in syndrome: Often caused by pontine lesions, if large can disrupt bilateral corticospinal tracts and abducens nuclei, eliminating body movements and horizontal eye movements. Sometimes vertical eye movements are preserved.

4. Optic radiation, Baum’s vs Meyer’s Loop:

vfd

Meyer’s Loop:

From the inferior retina, also called Archambault’s loop. Passes thru the temporal lobe by looping around the inferior horn of the lateral ventricle. Carries info of superior part of visual field. (Causes Pie in the sky defect of contralateral side).

Baum’s Loop:

From superior retina, travels straight back thru parietal lobe to occipital lobe in retrolenticular limb of internal capsule to visual cortex. Carries info from inferior part of visual field. Takes a shorter path, are less susceptible to damage. (Causes Pie in the floor defect of contralateral side).

meyersoptic rad

5. Location of visual cortices:

visualcor

Visual cortex receives radiation from lateral geniculate nucleus in the thalamus. Blood supply from calcarine branch of posterior cerebral artery.

cortices

Bonus material:

Pathways and locations associated with continued visual pursuit of an object:

associated

 

 

References:

https://psych.ucalgary.ca/PACE/VA-Lab/Brian/neuralbases.htm

https://healtheappointments.com/chapter-14-the-cranial-nerves-essays/4/

https://en.wikipedia.org/wiki/Internuclear_ophthalmoplegia

http://epomedicine.com/medical-students/horizontal-conjugate-gaze-pathway/

http://brain.phgy.queensu.ca/pare/assets/Oculomotor%20handout.pdf

http://www.opt.indiana.edu/v665/CD/CD_Version/CH9/CH9.HTM

http://www.library.med.utah.edu/NOVEL

http://www.msdmanuals.com/home/brain,-spinal-cord,-and-nerve-disorders/cranial-nerve-disorders/internuclear-ophthalmoplegia

https://emedicine.medscape.com/article/1215103-overview#a4

Who’s Eyeing You?

What’s This?

How would you like to learn? I choose to ask questions and then attempt to find the answers to them. Not all questions are answerable, but the right questions can lead to growth and comprehension.

I’ll try to categorize my questions if I’m able, but often I won’t be asking five questions on the same topic. The depth in which I answer each question will also vary, due to time constraints and limitations on the amount of personal understanding of the topic. I might repeat a question or go further in depth at some point, and my disclaimer is as follows: Information posted here is by no means authoritative. Use at own risk.
What’s This?