HEADACHE CASE REPORT

Presented by : Ade Mayashita

Moderator : dr. Yudiyanta, Sp.S(K)
Examiners : dr. Indra Sari Kusuma, Ph.D, Sp.S
Dr. dr. Cempaka Thursina, Sp.S(K)
Monday, November 20th, 2017
12.30 - 13.30

IDENTITY
Name : Mr. P
Age : 41 years old
Gender : Male
Religion : Moslem
Address : Sukoharjo, Jawa tengah
Occupation : Labourer
Education : Elementary school
Marital status : Married
Date of admission : September 23, 2017
Medical Record : 01.69.XX.XX

ANAMNESIS
Obtained from the patient

Chief Complaint : Headache

History of Present Illness

One month prior to admission, patient complained of high intensity, throbbing
headache in his right side of the head. He also vomited. Four days later, his right eyes
closed involuntary, and can not be opened. There was no problem with his sight. There is
blurred or doubled vision. He went to ophthalmologist and got eye drops for his
complained. He denied any weakness in the extremities, perioral numbness, hearing
problem, blurred or doubled vision, dysarthria, smelling problem, chocking, numbness or
weakness of extremities, seizure, decreased of consciousness, behavioral changes, urinary
problem.
Three weeks prior to admission, the patient still complained of headache. The right
eye closed. He went to neurologist, and asked to underwent head CT-scan. The result of
the CT-scan was edema cerebri. The patient was admitted to RSI Klaten for five days.
When the patient discharged, he was given mecobalamin 2 x 500 mcg, valisanbe 2 x 2 mg,
and Natrium Diclofenac 2 x 50 mg. The complained persisted.
Day of admission, the headache is getting more intense. The patient feels
continuous, high intensity, throbbing headache in the right side of his head. The right eyes
is still closed. Patient went to Sardjito Hospital. He denied any weakness in the extremities,
1
perioral numbness, hearing problem, blurred or doubled vision, dysarthria, smelling
problem, chocking, numbness or weakness of extremities, seizure, decreased of
consciousness, behavioral changes, urinary problem.

History of Past Illness

History of decrement of body weight within the last one month
Denied:
- History of previous headache
- History of trauma
- History of radiation/chemoptherapy/operation
- History of smoking
- Systemic medical conditions (autoimmune diseases)
- History of diabetes mellitus

- History of hipertension


- History of tumour
- History of high cholesterol
- History of cardiovascular problem
- History of • Long term medication

Family History
Denied:
- Tumor
- The same complaint

Social Economy History :

The patient is a labourer. He lives with his wife and three children. Patient has a good
relation with her family and relatives. Patient has middle-low economic status. Patient uses
BPJS as health insurance.

Systemic Anamnesis
- Cerebrospinal system : Subacute headache, non-proggresive, unilateral, throbbing,
severe intensity, closed right’s eyelid
- Cardiovascular system : no complaint
- Respiratory system : no complaint
- Gastrointestinal system : no complaint
- Musculoskeletal system : no complaint
- Urogenital system : no complaint
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- Integument system : no complaint

ANAMNESIS RESUME
A 41 years old with subacute, non-proggresive, unilateral, throbbing headache, and
closed right eyelid. Patient denied history of fever and trauma. Patient already underwent
head CT Scan in previous hospital with the result edema cerebri.

DISCUSSION I

Headache is pain or uncomfortable sensation in the area of the head with the the
lower border extend from chin to the area behind the head (the occipital region) and part of
the neck (PERDOSSI, 2013). The headache is a pain or discomfort in the head covering
face area and back the neck (Sjahrir, 2013). The patient felt pain in the right temple region.
Based on the location of the pain, clinically we may say that patient chief complaint is
headache.

Classification of Headache
Based on the International Headache Society (IHS) classification, The
International Classification of Headache Disorders, 3rd edition (ICHD-3, 2013):
1. Primary headache
- Migraine
- Tension-type headache
- Cluster headache and trigeminal autonomic cephalgia
- Another primary headache

2. Secondary headache:
- Headache associated with head and / or neck trauma
- Headache associated with cranial and / or cervical vascular disorders
- Headache associated with non-vascular disorder
- Headache associated with a substance or withdrawal process
- Headache associated with infection
- Headache associated with hemostasis disorders
- Headaches associated with cranial abnormalities, neck, eyes, ears, nose, sinus, teeth,
mouth or other facial or cranial structures
- Headaches associated with psychiatric abnormality
- Cranial neuralgia and facial pain central
- Headache, cranial neuralgia, central or other primary facial pain

According to the IHS criteria adopted by PERDOSSI, headache is differentiated

into primary and secondary headache. Ninety percent (90%) of headache is the primary
headache category, the remaining 10% fall into the category of secondary headache. The
term primary headache if there is no structural or metabolic damage underlying headache.
The term secondary headache when headache is based on structural or systemic damage
(PERDOSSI, 2013).
From anamnesis the patient had a subacute headache. Subacute because the
headache has been felt for 1 months (< 3 months). There is no progressivity, although the
patient felt severe-intensity headache. This Subacute headache accompanied by cranial
3
nerve palsy leads a suspicion of intracranial space-occupying lesion or a vascular origin.
Intracranial space occupying lesions may be neoplasm and non-neoplasm. The non-
neoplasmic lesion may be an intracranial infection (abscess), or a venous thrombosis.
Patient is in immunocompetent stage and deny the symptoms of infection such as history
of fever, chronic cough, weight loss, chronic cough, chronic diarrhea so that intracranial
lesions due to infection process can be excluded.

Cerebral Venous Thrombosis

Thrombosis of the venous channels in the brain is an uncommon cause of
cerebral infarction relative to arterial disease, but it is an important consideration because
of its potential morbidity. Lateral sinus thrombosis may be associated with headache and a
pseudotumor cerebri–like picture. Extension into the jugular bulb may cause jugular
foramen syndrome, while cranial nerve palsies may be seen in cavernous sinus thrombosis
as a compressive phenomenon. Cerebral hemorrhage also may be a presenting feature in
patients with venous sinus thrombosis.
The incidence of cerebral venous thrombosis (CVT) is difficult to determine, but
generally, it is believed to be an uncommon cause of stroke, with the reported ratio of
venous to arterial strokes being 1:62.5. In 1973, Towbin reported CVT in 9% of 182
autopsies, while in 1995, Daif reported a frequency in Saudi Arabia of 7 cases per 100,000
hospital patients. However, with the advent of newer imaging techniques, the reported
incidence of CVT is likely to increase as less severe cases are found.
Patients with cerebral venous thrombosis (CVT) may present with headache.
Although thunderclap headache usually indicates subarachnoid hemorrhage (SAH), it may
also be seen in sinus thrombosis. Patients with lateral sinus thrombosis may present with a
pseudotumor cerebri–like syndrome. Nausea and vomiting may also be associated with
CVT. In some cases, seizures, which can be recurrent, occur. Some patients may
experience a decreased level of consciousness that progresses to coma. Focal neurologic
deficit may develop, depending on the area involved. Hemiparesis may occur, and in some
cases of sagittal sinus thrombosis, weakness may develop in the lower extremity. This also
may occur as bilateral lower extremity involvement. Aphasia, ataxia, dizziness, chorea, and
hemianopia all have been described. Cranial nerve syndromes are seen with venous sinus
thrombosis.
Wasay et al found little association between headache location and the site of
sinus involvement in patients with CVT. In their study, the authors described the pattern
and location of headache in 200 consecutive patients with a proven diagnosis of CVT to
identify an association between the site of the headache and location of sinus involvement.
The quality of headache was reported as throbbing (9%), bandlike (20%), thunderclap
(5%), and other (pounding, exploding, stabbing, etc) (20%). The authors found no
association between headache location and the site of sinus thrombosis except in cases of
sigmoid sinus thrombosis, in which 17 of 28 patients (61%) with involvement of the
sigmoid sinus alone or in combination with the transverse sinus had pain in the occipital
and neck region. There was no association between lateralization of pain and the site of
thrombosis.

Brain Tumours

Brain tumors and headache are common and it is important to consider cerebral neoplasms
in any patient who has only headache as a symptom and no other significant neurologic

4
signs or symptoms. Many patients with headache and chronic daily headache have serious
secondary disorders and these need investigation. Headache can be a cardinal symptom of
serious disease, including primary cerebral neoplasms or metastatic disease. Headache is
present in 48% to 71% of brain tumor patients (Kirby, 2013).
Headaches are more common in brain tumor patients with a prior history of headache and
83% of patients noted an alteration in the character of their headache. The classic brain
tumor headache has been described as severe, early morning, or nocturnal headache
associated with nausea and vomiting but studies show that most brain tumor headaches are
nonspecific, intermittent, moderate to severe in intensity and progressive. The pain is
variably described as aching, pressure, tightness, and throbbing or shooting. Only 17% of
patients had classic brain tumor headaches (Kirby, 2013).
From the type of headache, the headache felt by the patient clinically migraine-like. Based
on the PERDOSSI criteria of 2013, the diagnostic criteria for migraine are:
A. At least headache lasts for 4-72 hours (untreated or already treated but not yet
improved)
B. Headache have at least two of the following characteristics:
1. Unilateral location
2. Pulsatile quality
3. Intensity of moderate or severe pain
4. Circumstances are exacerbated by physical activity or out of routine
physical activity (such as walking or stair climbing)
C. During headache, accompanied by one of the following:
1. Nausea and/or vomiting
2. Photophobia and phonophobia
D. Not related to other diseases

Most brain tumor headaches do not meet criteria for primary headache disorders.
Up to 15% of patients report migraine-type headaches but these usually have atypical
features. Tension-type headaches are reported in 29% to 39% of patients. The frequency of
headaches depends on the location of the tumor. More than 90% of patients with
intraventricular and midline tumors had headache. With infratentorial tumors, 70% to 84%
of patients had headaches versus 55% to 60% of patients with supratentorial tumors.
Factors that may increase the risk of headache include raised intracranial pressure, degree
of midline shift and increasing edema (Kirby, 2013). Tumor pathology also may affect the
likelihood of headache. Slow-growing tumors may be less likely to cause headache
because there is more time for the pain-sensitive structures to adapt than with a fast-
growing tumor and usually there is less associated cerebral edema.
Headache may appear as one of the symptoms of intracranial neoplasm, which is
about 25% of patients with intracranial neoplasms. The intensity of the pain can be mild to
severe, sharp or dull, and appears episodically. Typical symptoms are appearing or worsen
at night or appearing when the patient wakes up first in the morning. If the vomiting
appears when the peak intensity of headache, it also high suspicioun of intracranial tumor
headache. Headache in intracranial neoplasm is likely due to the effect of shifting,
stretching or stretching of blood vessels and duramater structures and this process may
appear long before the rise of intracranial pressure (Ropper, 2014).
Based on the origin of the cell, intracranial neoplasms can be distinguished
primary and secondary (metastatic) neoplasms. Epidemiologically, metastatic intracranial
neoplasms are more likely to be incidentally found than in primary intracranial neoplasms.

5
The source of intracranial metastasis is often from the breast, lungs, kidneys and melanoma
(Ropper, 2014). In adulthood, primary epidemiologic primary intracranial neoplasms are
derived from astrocytes (astrocytoma, glioblastoma multiform) and meninges
(meningioma).

TEMPORARY DIAGNOSIS
Clinical diagnosis : subacute non-progressive unilateral, throbbing, severe intensity
headache, closed right’s eyelid
Topical diagnosis : Intracranial pain sensitive structure
Etiology diagnosis : Cerebral Venous Thrombosis dd brain tumour

PHYSICAL EXAMINATION
General State
General appearance : Good, Weight: 50 kg, Height: 158 cm, BMI: 21
Level of Consciousness : CM, GCS E4V5M6
Vital Sign : BP : 149/93 mmHg
HR : 86 x/minute
RR : 20 x/minute
t : 36,7o C
NPS : 9
Head : Mesocephal, deformity (-), nasal discharge (-), ear discharge (-),
anemic conjunctiva, non-icteric sclera
Neck : JVP not elevated, lymph node impalpable
Chest
- Lungs : I : Symmetrical
Pa : Tactile fremitus right = left
Pe : Sonor in all chest wall
Au : Vesicular lung sounds, vesicular right = left
- Heart : I : Ictus cordis can’t be identified
Pa : Ictus cordis felt 2 cm medially to left midclavicular line
Pe : Heart configuration within normal limit
Au : Heart sounds I – II pure, gallop (-), murmur (-)
Abdomen : I : Flat
Au : normal bowel sounds (+)
Pe : Tympany,shifting dullness (-),unilateral dullness (+) normal
Pa : Soft, non-tender, hepar and spleen impalpable
Extremity : edema (-), muscles atrophy (-)
Integumentum : within normal limit

Neurological Status
Body position : straight and symmetrical
Gait : normal
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Head : mesocephal
Right Left
N.I Smell sense Within normal limit Within normal limit
Visual function >3/60 >3/60
Color Vision Within normal limit Within normal limit
N.II
Eye field Within normal limit Within normal limit
Fundus Within normal limit Within normal limit
Ptosis + -
Eye movement to the medial Paralysed Within normal limit
Eye movement to the superior Paralysed Within normal limit
Eye movement to the inferior Paralysed Within normal limit
N.III
Pupil size 5 mm 3 mm
Direct light reflex + +
Consensual light reflex + +
Divergen strabismus - -
Eye movement to the lower lateral Paralysed Within normal limit
N.IV
Convergen strabismus - -
Biting Within normal limit Within normal limit
Mouth opening Within normal limit Within normal limit
st
N.V Face sensibility Paralysed in 1 branch Within normal limit
Corneal reflex + +
Trismus - -
Eye movement to the lateral Paralysed Within normal limit
N.VI
Convergen Strabismus - -
Eye blink Within normal limit cant be evaluated
Nasolabial fold Within normal limit Within normal limit
Mouth corner Within normal limit Within normal limit
Forehead Wrinkling Within normal limit Within normal limit
Eye closing Within normal limit closed
N.VII Grimace Within normal limit Within normal limit
Cheek puffing out Within normal limit Within normal limit
Taste sense on 2/3 anterior tongue Within normal limit Within normal limit
Glabella reflex - -
Myerson sign - -
Chovstek sign - -
Hearing whisper Within normal limit Within normal limit
Hearing clock’s ticking Within normal limit Within normal limit
N.VIII Rinne test Within normal limit Within normal limit
Schawabach test Within normal limit Within normal limit
Weber test Within normal limit Within normal limit
Pharyngeal arc Within normal limit
Taste sense on 1/3 posterior tongue Within normal limit Within normal limit
N.IX
Gag reflex + +
Nasal sound - -
Heart rate 86 x / min, regular 86 x / min, regular
N.X Pharyngeal arc Within normal limit
Voice Within normal limit Within normal limit
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 Swallowing Within normal limit
Head turning Within normal limit Within normal limit
Shoulder position Within normal limit Within normal limit
N.XI
Shoulder lifting Within normal limit Within normal limit
Shoulder muscle trophy Within normal limit Within normal limit
Tongue position within normal limit
Articulation Within normal limit Within normal limit
Tongue tremor Within normal limit Within normal limit
N.XII
Tongue protruded within normal limit
Tongue muscle trophy Within normal limit Within normal limit
Tongue fasciculation - -

Neck : Meningeal sign (-)

Extremities :
M N N S 5 5
N N 5 5

Fr +2 +2 Pr - -
+2 +2 - -

Tn N N Tr N N Cl - -
N N N N

Spesific Local Examination:

Pericranial tenderness : negative
Trigger point : negative
Lhermite sign : negative
Spurling sign : negative
Distraction test : negative

Neurooptahlmology examination: funduscopy within normal limit

MMSE : 28 (Normal cognitive function)

MOCA-Ina : 29 (Normal cognitive function)
ADL : 0 (Independent)
IADL : 0 (Independent)
KPS : 90 (Normal daily function and no need special treatment)
Barthel Index : 100 (Independent)
HDRS : 0 (No Depression)
HARS : 1 (No Anxiety)
GI Risk : Low risk
CV Risk : Low cardiovascular risk

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Sensibility : hypoesthesia in 1st branch of nerves no. V
Vegetative : within normal limit

PHYSICAL EXAMINATION RESUME

- General appearance normal, CM, hypertension, paralysis nervus III, IV, V branch
no I, VI UMN

SUPPORTING EXAMINATION

LABORATORY EXAMINATION

30/9/2017 1/10/2017 19/9/2016

Complete Blood Count Complete Blood Count
Hemoglobin 12,3 g/dL Uric Acid 5,0 mg/dL Hemoglobin 11 g/dL
Leucocytes 13,91 X 103/µL Fasting 97 mg/dL Leucocytes 14,5 X 103/µL
glucose

9
Erithrocytes 4,43 X 106/µL Total Chol 175 mg/dL Erithrocytes 4,3 X 106/µL
Platelet 286 X 103/µL HDL 89 mg/dL Platelet 398 X 103/µL
Haematocrit 37,9 % Trigliserid 60 mg/dL Haematocrit 35,4 %
Neutrophil 79,5 % LDL 92 mg/dL Neutrophil 83 %
Lymphocyte 13,2 % HbA1c 5,2 % Lymphocyte 13,3 %
Monocyte 6% Monocyte 2,5 %
Eosinophil 0,9 % Eosinophil 0,1 %
Basophil 0,4% Basophil 0,02 %
Chemical Blood Test Chemical Blood Test
BUN 16 mg/dl (Urin Rutin) BUN 18,2 mg/dl
Creatinine 0,67 mg/dl Creatinine 0,78 mg/dl
Albumin 4,65 Albumin 3,7 mmol/L
Sodium 139 mmol/L Sodium 144 mmol/L
Potassium 3,75 mmol/L Potassium 3,61 mmol/L
Chloride 103 mmol/L Chloride 106 mmol/L
SGOT 14 U/L SGOT 10 U/L
SGPT 23 U/L SGPT 18 U/L
Blood 86 mg/dL Blood 108 mg/dL
Glucose Glucose
Haemostatic functon
PPT 15,2 detik PPT 12,9 detik
INR 1,12 INR 0,92
APTT 28,6 APTT 25,8

EKG (September, 22th 2017)

EKG:

Normal sinus rhytm

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Thoracic x-ray (September, 22th 2017)

Impression:

- Lung within normal limit

- Cor within normal limit

Head CT Scan with contrast (August, 28th 2017)

Impression:

- Edema cerebri

9
MRI (September, 28th 2017)

Impression:

- Soft tissue mass in the lateral sphenoidalis dextra that extend to the
sphenopalatina foramen, and destruct the craniolateral wall pf sphenoidalis
sinus susp glioma dd meningioma
- Susp. Thrombosis of the left transversus sinus and left sigmoid sinus
- Hipoplasia of vertebral arteries dextra segmen 2-4
- There is no sign of infarction, haemorrhage, intracranial space occupying lesion
- There is no sign of increased intracranial pressure

Arteriography of vertebral arteries (October 17th 2017)

2
Impression:

- Thrombus in the sigmoideus sinus sinistra

- Hipervascularity in the lateral internal carotis artery dextra pars cavernous
susp. Parasellar dextra mass, lateral from the cavernous sinus dextra

Consultation:
- Neuroseurgeon (October 3rd, 2017)
Assesment : Left sphenoid wing meningioma DD Arterivenous Malformation
Plan : Craniotomy removal tumor
- Neurosurgeon Operation Report (October 10th, 2017)
 Craniotomy removal tumor
 Macroscopic : Solid tumor tissue with firm borders and tumor bed in
sphenoid wing. Removal tumor Simpson grade II.
 Post operative diagnosis: Left sphenoid wing meningioma
- Pathology Anatomy (October 17th 2017)
 Left Temporal Base tumor
 Transitional Psammomatous Meningioma (WHO grade I)

DISCUSSION II
Salivary gland tumors represent 3-10% of all head and neck neoplasms.1 These
tumors occur predominantly in major salivary glands (Bittar et al, 2015)..2,3 The parotid
gland is affected most often, ranging from 36.6% to 83%. Malignant tumors are a
minority, occurring in 15-32% of cases. The most common malignant and benign tumors
are the mucoepidermoid carcinoma and the pleomorphic adenoma, respectively. The
pleomorphic adenoma comprises 45-60% of all salivary gland tumors. Approximately 80%
occur in the parotid gland, usually in the inferior pole of the superficial lobe; however, less
frequently, it can occur at the deep lobe or in the accessory parotid tissue. Several surgical
approaches have been described to treat this tumor. In 1895, Senn described enucleation as
the technique of choice. However, tumor removal was incomplete with an unacceptable
rate of recurrence (Bittar et al, 2015).

3
 Total parotidectomy removes all gland tissue lateral and medial to facial nerve,
whereas superficial parotidectomy removes parotid gland lateral to the facial nerve. In
extra- capsular dissection, it is not performed any dissection of the facial nerve (Roh et al,
2007). The risk of facial nerve trauma during surgery increases for recurrent tumours and
in total parotidectomy, where deep lobe is also removed. The most common complication
of parotid surgery is facial nerve palsy, particularly of the marginal mandibular nerve.
Lesion of the facial nerve is one of the most serious complications that can occur in
parotid gland surgery (Bittar et al, 2015). It is estimated that 30-65% of all patients
experience some sort of transient facial weakness, and 3-6% evolve with permanent
dysfunction resulting in significant impact in the quality of life (Bittar et al, 2015).
Facial nerve injury mechanisms during parotidectomy include nerve division,
stretch, compression, ligature entrapment, thermal and electrical injuries, and ischemia
(Bittar et al, 2015).

Postoperative follow-up of facial nerve function was carried out using the House–
Brackmann grading system. is scoring system includes six grades based on the degree of
FN function: grade I is normal nerve function; grade II indicates mild nerve dysfunction
not detectable at rest; and grades III–VI indicate progressively severe paresis of the nerve

4
in function and at rest (Fareed et al, 2014). All patients were followed up weekly for 1
month, then monthly for 6 months, or to full recovery (Fareed et al, 2014).

Under normal circumstances, the nerves remain connected with their innervation
targets during the whole life of an individual. The most common disturbance to this status
quo is a nerve damage by mechanical forces, which results in a loss of ability of the nerve
to transfer stimuli (Madura, 2012). These forces can act through compression, traction,
laceration and direct injection into the nerve. Moreover, the nerve can get damaged by
thermal noxae, electric current, radiation and metabolic disorders. As a result of the injury
the CNS completely, or partially, looses the ability to communicate with the neural end
organs. The extent to which this happens is greatly variable and depends on the degree of
damage to the nerve. The first classification of the severity of nerve injury was published
by Seddon and was based on his extensive experience with war victims. He classified the
nerve injuries to three degrees, neuropraxia, axonotmesis and neurotmesis and defined the
terms as follows:

1. Neurotmesis describes the state of a nerve in which all essential structures have
been sundered. There is not necessarily an obvious anatomical gap in the nerve;
indeed, the epineural sheath may appear to be in continuity, although the rest of the
nerve at the site of damage has been completely replaced by fibrous tissue. But the
effect is the same as if anatomical continuity had been lost. Neurotmesis is
therefore of wider applicability than division.
2. Axonotmesis—here the essential lesion is damage to the nerve fibers of such
severity that complete peripheral degeneration follows; and yet the epineurium and
more intimate supporting structures of the nerve have been so little disturbed that
the internal architecture is fairly well preserved. Recovery is spontaneous, and of

5
 good quality, because the regenerating fibers are guided into their proper paths by
their intact sheaths.
3. Neuropraxia is used to describe those cases in which paralysis occurs in the
absence of peripheral degeneration. It is more accurate than transient block in that
the paralysis is often of considerable duration, though recovery always occurs in a
shorter time than would be required after complete Wallerian degeneration; it is
invariably complete.

Neuropraxia

Neuropraxia is a situation where the nerve (or more commonly a segment of it)
losses its ability to propagate action potential while the structural continuity of the axons is
fully preserved. The condition is associated with segmental demyelination of the nerve
fibers. Because the degree of myelination differs depending on the type of nerve fibers, so
does the extent of functional loss and return. The motor fibers are the most susceptible and
their function is lost first and regained last, whereas pain and sympathetic fibers are the
opposite (Madura, 2012). Typical example of this type of nerve injury is sleeping with the
pressure on the nerve, also called the “Saturday night palsy”. This type of injury usually
recovers within 12 weeks without any intervention.

Axonotmesis

Axonotmesis is an injury resulting in the loss of axonal continuity without any

damage to the connective tissue structures within the nerve. Full Wallerian degeneration
and axonal regrowth occur here and a Tinnel’s sign accompanies the regeneration. The
recovery of function is usually very good, although not as good as in neuropraxia. Surgical
intervention is normally not necessary (Madura, 2012).

Neurotmesis

Damage to the neural connective tissue structures, including endoneurium,

perineurium and / or epineurium is termed neurotmesis. Again, Wallerian degeneration and
axonal regrowth occur and Tinnel’s sign is possible to elicit over the injured nerve. The
regeneration process here is hampered by axonal misdirection, loss of nerve/blood barrier
and intraneural scarring. Injuries interrupting peri- and epineurium require surgical
intervention. The outcome is generally worse than in axonotmesis. This, however, also
depends on the relative location from the innervation target and in general it is difficult to
predict (Madura, 2012).

Early work of Sunderland brought about a much deeper understanding of the nerve
ultrastructure (Sunderland, 1947, Sunderland and Bradley 1949). This offered an
explanation for a wide variety of clinical findings and outcomes in the neurotmesis
category. Natural following of this line of thought was extension of the Seddon’s
classification, which was formalised by Sutherland (Sunderland 1978). In the new
classification the types I and II correspond to neuropraxia and axonotmesis respectively.
6
Type III is an injury involving axons and endoneurium while perineurial and epineurial
structures are intact. Sunderland’s type IV injury is associated with division of axon,
endoneurial and perineurial structures. This is a more significant injury, which often leads
to intraneural scarring and requires surgical intervention to ensure the best possible
outcome. Finally, type V of Sunderland’s classification is a total division of the nerve
trunk where all the neuronal and connective tissue structures are interrupted. It is important
to note that in real clinical situation nerve injury is often a combination of more than one
type of injury. This mixed pattern injury has been classed as a type VI, which was added to
the original classification at a later date .Correlations among the grade of injury, clinical
and electrophysiological findings and potential for functional recovery , The correlations
are found in the following Table 1:

Seddon Neuropraxia Axonotmesis Neurotmesis Neurotmesis Neurotmesis

Sunderland Type I Type II Type III Type IV Type V
Anatomical Axonal,
Axonal
continuity Axonal and endoneurium
continuity Complete
Pathological preserved endoneurium and
disrupted division of
findings Selective continuity perineurium
(together with the nerve
demyelination of disrupted continuity
myelin sheath)
the injury zone disrupted
Wallerian
No Yes Yes Yes Yes
degeneration
Motor
Complete Complete Complete Complete Complete
paralysis
Sensory Often partially
Complete Complete Complete Complete
paralysis spared
Autonomic Much of the
Complete Complete Complete Complete
paralysis function spared
Muscle Progressive Progressive Progressive Progressive
Very little
atrophy with time with time with time with time

7
Seddon Neuropraxia Axonotmesis Neurotmesis Neurotmesis Neurotmesis
Sunderland Type I Type II Type III Type IV Type V
Tinnel’s sign Absent Present Present Present Present
Normal
conduction
proximal and
distal to
No conduction No conduction No conduction No conduction
injury site
Electrophysiol distal to injury distal to injury distal to injury distal to injury
No
ogical findings site Fibrilation site Fibrilation site Fibrilation site Fibrilation
conduction
waves present waves present waves present waves present
through injury
site
No fibrilation
waves

8
Spontaneous
Complete Complete Variable None None
recovery
Surgery
No No Varies Yes Yes
needed?
Only after Only after
Rate of Days (up to 3 Slow – 1 mm Slow – 1 mm surgical repair surgical repair
recovery months) per day per day - 1 mm per - 1 mm per
day day

Table 1. Classifications of nerve injuries and their correlation with clinical, pathological
and electrophysiological findings.

FINAL DIAGNOSIS
Clinical diagnosis : chronic non-progressive paresis of facialis nerve lower motor
neuron type
Topical diagnosis : Peripheral Facialis nerve sinistra
Etiology diagnosis : Iatrogenic

Therapy
During surgery, the facial nerve can be bruised, stretched or cut. When this
happens the nerve will not send messages to the muscles properly. This can result in
problems with facial movement such as a floppy cheek, droopy mouth or issues with eye
closure (NHS, 2017). Sometimes we do not know for certain whether the nerve is just
bruised or whether it is more severely damaged. The key principles for early management
of facial weakness are:

1) Aim for symmetry at rest

2) Mouth care

3) ‘Normal’ eating and talking

4) Eye care

5) Gentle stretches

6) Massage

7) Gentle exercises

The goals of this early management are to try to reduce the likelihood of
developing longer term problems and to promote good conditions for nerve recovery

9
(NHS, 2017).

Drugs to promote recovery of nerve damage is mecobalamin. It is often used to accelerate

recovery of peripheral nerves (Gan et al, 201).

Mecobalamin promotes functional and morphological recovery after peripheral nerve

injury. The molecular mechanism underlying the restorative effects of mecobalamin on
injured nerves may involve upregulation of the genes for multiple neurotrophic factors
(Gan et al, 2014). The signaling pathway through which mecobalamin acts to promote
peripheral nerve regeneration remains to be investigated in the future (Gan et al, 2014).

1. Non Pharmacology
- Physiotherapy
2. Pharmacology
- Mecobalamin 2x 500 mcg
- Folic acid 2x1 tab

PROGNOSIS
Facial nerve injury during superficial parotidectomy remains the most common and
most feared complication. In a study (Bittar et al, 2015) found that tumors with 3.0cm or
more in length and/or 2.0cm or more in depth have a significant higher risk of facial nerve
injury. Secondary surgery to recurrent tumors also has a much higher risk of evolving with
facial palsy after superficial parotidectomy (Bittar et al, 2015). Crushing or stretching
injury causes interruption in nerve electric conduction and is similar to axonotmesis, which
recovers in a period of 3-6 months. Stretching injury recovers slower than crushing injury
as they differ in range and degree. Divisional injury shows complete interruption of nerve
conduction and are akin to neurotmesis which recovers after six months of injury8.
Frequency of permanent facial palsy in a series was 1.7% whereas in other studies it
ranges from 2% to 10% and 11% (Musani et al, 2014). However, Gaillard et al. found no
facial weakness after 6 months in his study of 131 benign parotid surgeries. It is in
accordance with the literature which shows 0 - 10% rate of permanent facial weakness.
Temporary paresis usually resolves, according to Laccourreye, within the 18th post-
operative month (Ragona, 2005).

1. Death : ad bonam
2. Disease : ad bonam
3. Discomfort : dubia ad bonam

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4. Dissatisfaction : dubia ad malam
5. Disability : dubia ad bonam
6. Destitution : dubia ad bonam

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 Bibliography
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analysis of possible predictors of this complication. Braz J Otorhinolaryngol, 82:447-51.
Dulguerov P, Marchal F, Lehmann W. 1999. Postoperative facial nerve paralysis: possible
etiological factors and results with routine facial nerve monitoring. Laryngoscope;
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Fareed M, Mowaphy K, Abdullah H, Mustafa M. 2014 . Temporary facial nerve paralysis after
parotidectomy: the mansoura experience, a prospective study. 2014 The Egyptian Journal
of Surgery 1110-1121.
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role of local factors. Laryngoscope. 115:287-91.
Gan L, Qian M, Shi K, Chen G, Gu Y, Du W, Zhu G. 2014. Restorative effect and mechanism of
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Kim J, Armenia A. 2016. Facial Nerve Paralysis. Medscape Updated: Mar 07, 2016
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BMJ;351:h3725.
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for Benign Parotid Tumours .Journal of the College of Physicians and Surgeons Pakistan,
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NHS Foundation Trust. 2017. Early management of post operative facial weakness. Leaflet
number: 3765/VER2. www.facialpalsy.org.uk.
Ragona, Marchese. 2005. Treatment of complications of parotid gland surgery.ACTA
OTORHINOLARYNGOL ITAL 25, 174-178.
Roh JL, Kim HS, Park CI. 2007. Randomized clinical trial comparing partial parotidectomy
versus superficial or total parotidectomy. Br J Surg. 94:1081-7.
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Senn N. 1895. The pathology and surgical treatment of tumors. Philadelphia, PA: W.B. Saunders
Sunderland, S, and K C Bradley. 1949. “The cross-sectional area of peripheral nerve trunks
devoted to nerve fibers.” Brain: A Journal of Neurology 72 (3) (September): 428-449.

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Sunderland, Sydney. 1978. Nerves and nerve injuries. 2nd ed. Edinburgh; New York: Churchill
Livingstone; distributed by Longman.
Tomas Madura. 2012. Pathophysiology of Peripheral Nerve Injury, Basic Principles of Peripheral
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disorders/pathophysiology-of- peripheral-nerve-injury.
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