Headaches Flashcards
e.g. Migraine, Tension Headache
Post-Traumatic Headache (PTH)
-> Definition + Etiology
PTH = a type of Secondary Headache
PTH =
Headache occurring in the days after a head injury or after regaining consciousness
Etiology:
PTH is a complication of..
- Traumatic Brain Injury (TBI)
- Whiplash injury (= Schleudertrauma)
- Craniotomy
Post-Concussive Syndrome
MODERATE or SEVERE Traumatic Brain Injury
Associated with:
1) Loss of consciousness for >30min
2) Glasgow Coma Scale (GCS) <13
3) Post-traumatic amnesia for > 24h
4) Altered Level of Consc. for > 24 h
5) Imaging positive for traumat. Head
injury -> e.g:
- Skull fracture,
- Intracranial Haemorrhage
- and/or Brain contusio
MILD Traumatic Brain Injury (mTBI)
Associated with NONE of the following
(= S&S of Moderate or Severe TBI):
a) Loss of consciousness for > 30min
b) Glasgow Coma Scale (GCS) <13
c) Post-traumatic amnesia for > 24h
d) Altered Level of Consc. for > 24 h
e) Imaging positive for traumat. Head
injury -> e.g:
- Skull fracture,
- Intracranial Haemorrhage
- and/or Brain contusio
Associated with MIND.1 of the following:
a) Transient confusion, disorientation, impaired consciousness
b) Memory loss for events immediately before / after injury
c) >2 of following Symptoms:
i. nausea
ii. vomiting
iii. visual disturbances
iv. dizziness and/or vertigo
v. gait and/or postural imbalance
vi. impaired memory and/or concentr.
Post-Traumatic Headache (PTH):
Diagnostic criteria & Types
PTH-Diagnosis is mostly based on Clinical criteria:
ACUTE PTH
- Onset of Headache within 7d after the head or neck trauma
- Remitting within 3 months after the onset
PERSISTENT PTH
(same as Acute =) Onset of Headache
within 7 d after head or neck trauma,
Persisting for > 3 months after onset
Secondary Headaches:
Venous Thrombosis
Symptoms, incl. Headache, depend on:
o Which Venous tract is involved?
-> Cortical veins vs. Venous sinuses
o How many vascular districts are affected?
-> limited vs. diffuse
o How fast does Thrombosis develop?
-> can collateral circuits be activated?
Secondary Headaches: Subarachnoid Hemorrhages (SAH)
SAH = dangerous bc autonomic symptoms (brady+tachyk, hypertension, vasospasms)
-> death within 15min
SAH & Headache as symptom:
o Thunderclub Headache in 97% of cases = very sudden / acute onset Headache
o Warning / Sentinel Headache
= Headache that rapidly disappears
-> occurs in case of:
i. Micro-bleeding
ii. Enlargement of the Aneurysm
iii. Intramural bleeding
iv. Vasospasm
v. Micro-embolic phenomena due to Intrasaccular clots
Secondary Headaches:
1. Vascular Intracranial / Cervical disorders
1) Hematomas:
-> Intracerebral, Subdural, Epidural
2) Subarachnoid Hemorrhages*
3) Venous Thrombosis*
4) Vascular Malformations in pre-clinical stage:
o Saccular Aneurysms
o AV-Malformations
Secondary Headaches: Vascular malformations in pre-clinical stage
o Saccular Aneurysm
o AV-Malformation
Secondary Headaches - Underlying disorders
= 9
- Vascular Intracranial / Cervical disorders*:
i. Hematomas
ii. Subarachnoid Hemorrhage
iii. Venous Thrombosis
iv. Vascular malformations in pre-clinical stage - Non-vascular intracranial disorders (= space occupying: Granulomata, Cysts)
- Trauma to Head / Neck
- Substance abuse / withdrawal
- Pathologies of other structures of the head (ears, eyes, teeth etc.)
- Infections: Meningitis, Encephalitis
- Disorders of Homeostasis:
Kidney, Liver, Respiratory insufficiency - Psychiatric disorders: Depression, Psychosis
- Brain Tumor:
Headache is an Onset symptom in 35%, but rarely occurs isolated
= more likely in pts who already have a Primary Headache history
Secondary Headaches Def
Headache that is a symptom of an underlying disease*
Other Primary Headache Diseases
Arnold-Chiari’s Malformation:
Cerebellar tonsils are positioned more downwards, can penetrate into the Foramen Magnum
-> with time can lead to compression of the
anteriorly located Brainstem -> e.g.
- Bulbar part containing Breathing center
- Swallowing center
S&S:
- very frequent Headaches = bilateral & located posteriorly
- contraction of the Occipital Peri-cranial muscles
- if Brainstem compressed => impaired swallowing, breathing, reduced level of consciousness
Treatment: must be corrected surgically
Migraine Pathophysiology - Further contributions:
1) Interplay with Reticular Formation:
Locus Coerulus = major site of Catecholamine synthesis (wsl. reason for Autonomic symptoms in Migraine)
Raphe Nuclei → decreased Serotonin levels (→ Depression + Anxiety = common Migraine comorbidities)
2) Hypothalamic activation in the Prodromic Phase → explains associated Symptoms: Polyuria, Mood changes, Appetite changes
3) Activation of Temporal + Occipital Cortex
→ explains Photophobia
Medication Overuse Headache - Treatment
=> Withdrawal of overused medication
=> + Preventive medication
Advice itself is effective in > 50%, other possibility is Withdrawal programe (Hospital- / Home based)
Outcomes
in 80%: Resolution of Medication overuse
in 50%: Reduction of monthly Headache days to <50%
in 70%: Reversion to Episodic Migraine (<15 Monthly Migraine Days)
in 35%: Relapse of MOH
Medication Overuse Headache - Diagnosis
consider NEUROIMAGING
PSYCHOLOGICAL assessment, bc:
- Med. Overuse Headache has high comorbidity with Anxiety + Depression
- to determine the Overuse-pattern (addiction vs. “simple” overuse)
Medication Overuse Headache - Def
= Type of Headache that develops + gets worse with frequent use of Medications = most often Acute Headache Medications, against pain in Migraine- or TTH-pts
-> underlying Headache disorders transform from Episodic conditions to Chronic Daily Headache
-> 15 Headache days / month (i.e. Chronic)
General Pathophysiology of Headaches
The Brain parenchyma itself does not have pain receptors!
Instead, pain originates in Algogenic (pain producing) structures in the Head:
● Scalp skin + vessels
● Head + Neck muscles
● Venous sinuses
● Meningeal + large Cerebral Arteries
● Dura Mater at the cranial base
● Nerve fibers: CN V + IX + X
● Non-neurological structures in Head: teeth, oral mucosa, paranasal sinuses, eyes, ears**
Cluster Headache - Treatment
● Acute attacks:
o Oxygen administration (FiO2 of 100%)
o Sumatriptan (5-HT1 receptor blocker), via nasal spray or IV
● Prophylactic treatment:
o Short-term (for Episodic CH) – Prednisone, Verapamil (CCB)
o Long-term (episodic + chronic CH) – Verapamil, Lithium
(Verapamil -> ECG monitoring mandatory, bc risk for prolonged PR segment)
● Neurostimulation therapy (DBS)
o when medical therapy fails
o There are less invasive methods by stimulating the occipital nerve, sphenopalatine ganglion or the vagus nerve
Secondary Headaches
= Headache is a symptom of an underlying disease:
o Trauma to Head and / or Neck
o intracranial / cervical Vascular disorder: Hemorrhage, Venous Thrombosis
o Non-vascular intracranial disorder: cyst, granuloma (= space occupying)
o Substance Abuse or Withdrawal
o Infections: Meningitis, Encephalitis
o Disorder of Homeostasis = imbalance of ions or metabolites: Liver / Kidney / Respiratory Insufficiency
o Pathologies of structures of Head: eyes, ears, nose, sinuses, teeth, oral mucosa
o Psychiatric disorders: depression, psychosis
o Brain Tumors:
Headache = onset symptom in 30-40% of cases, but it rarely comes isolated;
more common in pts with history of Primary Headaches
Cranial Neuralgia
= Nerve Pain
-> Pain follows CN territories (eg. CN V) or Roots of C1 / C2
Neuropathy refers to nerve damage Neuralgia is a type of Nerve pain. Neuralgia can be a symptom of neuropathy
Types of Headache
Primary H.
Secondary H*
Painful Cranial Neuropathies (e.g. Cranial Neuralgias*), other Facial pains
Comorbidities & Epidemiology in Primary Headache Types
Bild
Characteristics of the different Types of Primary Headache
- Duration*
- Pain features (siehe Bild)
İ. intensity
ii. quality
iii. side
iv. location
v. Autonomic symptoms?
vi. Other accompanying symptoms
vii. Aggravated by physical activity? - Comorbidities*
- Epidemiology
- Treatment
- Other additional characteristics
Diagnosis Primary Headaches
- Diagnostic Algorithm: Primary vs. Secondary Headache (KK)
- HISTORY
i. Family History -> in Migraine usually parents are affected
ii. Medical History
o Past -> TTH: Hypertension, Mood disorders
o Recent: Stroke, Trauma, Intracranial surgery
iii. Natural History: was the Headache present/absent during important developmental periods?
(eg. females -> puberty, menopause)
- Pain features*
- General Medical examination
- Neurological examination
- İnstrumental examination
Primary Headaches - Diagnostic Algorithm
Primary Headache = when there are..
1. NO Alarm signs =>
i. Fever
ii. Focal Neurological Deficits
(->mein Notion)
iii. Seizure
iv. Meningeal signs (e.g. Nuchal rigidity)
v. Elevated ICP - signs (e.g. Papilledema)
vi. Decr. Level of Consciousness
-
NO Abnormal examination
=> Medical & Neurological examination -
NO Unusual features =>
e.g. we visit pt later and now they show Somatosensory dysfunction
DD Cluster Headache
Trigeminal Neuralgia => attacks are localized more in the Maxillary / Mandibular area
Sinusitis => is as well a disease with seasonal occurrence, but pain is less severe& worsens while bending forward
Migraine => as well unilateral, but Migraine pts prefer not to move and stay in a dark room, attacks last longer (4-72h), different Autonomic symptoms
Parosysmal Hemicrania (another TAC Type) = very similar to Cluster, but there have to be mind. 20 attacks for Diagnosis, lasting 2-30 min (vs. 15-180 min in CH)
Pathophysiology Trigem. Autonomic Cephalgias (TACs) PERIPHERAL component 1/2
- Peripheral component
= Activation of the following Nerve Fibres in the Cavernous Sinus:
İ. Fibers running from the Sphenopalatine ganglion to the Superior Salivary Nucleus (Brainstem)
ii. Fibers running from the Trigemınal ganglion to the Trigeminal Nuclei (Pons)
iii. Fibers running to Super. Cervical ganglion, then to the Medio-lateral Columns in Spinal Cord