Psychiatrist explains "Benzo Injury".

Being part of the prescribed harm community for many years we have lost many to suicide due to benzo withdrawals.

It’s as if we shouldn’t get prescribed it in the first place

Quitting benzos should not cost $30,000-$40,000. Period. Any MD should be able to taper a patient off of benzos. You can do it with BenzoBuddies for free.

I have to wear the same glasses now.

Geeeese, they should never be prescribed long term. And upto 20% causing this injury? The deprescribing guideline needs to be changed, surely. Is there not another medication that acts on GABA that can soften the withdrawals? I think that there is.. but would require supervision! If someone has been severely attacked, or something extreme has happened cause acute PTSD... then PRN *rescue* pills are suitable and the kindest thing to do... and often the only effective thing (as talking therapy actually makes it worse). Long term makes no sense, due to tolerance and lack of having a plan. Sadly, due to the long term harms and dependence some peopole experience with LONG term use/daily use... the pendulum has swung too far the other way so that patients who are in real need of a short-term PRN rescue course (ie 7-10 tablets for a month or 3 months, following something like being terrorized/home invasion & r_pe/ trafficking etc) will have physicians refuse to prescribe them, even when recommended by another assessor. A serious lack of common sense and that someone taking 5 doses in 2 months cannot possibly get any physical dependency. Just knowing that have them can be a psychological crutch in case of a major trigger and 8 hours of shaking, dry mouth, and feeling horrendous. There is no alternative. Beta-blockers do not work for persons in a REAL rational state of terror/trauma. Hence why many persons end up self-medicating with ETOH. Worse still, the system pathologizes victims -- and in the worst scenarios the system is weaponised to silence, smear, and discredit key witnesses.

I quit Xanax cold turkey and it was worse then coming off opiates. I thought people were outside watching me coming to get my daughter.. I didn’t feel right for a year!!

Oy vey.

I respectfully suggest the 18-24 month recovery is plausibly too generous if Benzos taken as prescribed for a decade+, or have specific genetic variants influencing calcium (Ca) regulation, or if took Benzos as Rx’d with other meds. A fascinating glimpse into realities of long-term benzo use (taken as Rx’d) shows overlapping characteristics between Benzo WD & Stiff Person Syndrome. Watch symptom flare timing thru intradose withdrawal lens (benzo wearing off before next scheduled dose). 🤯 Fascinating documentary inadvertently demonstrating flare timing: time stamps provided in @celinedion’s Documentary without specifying Benzo played plausible role in subsequent SPS. Timestamps & clinical symptom manifestation are undeniably characteristic of acquired Channelopathy Ca dysregulation triggering tetany-like full-body seizures as well as stiffness assoc’d w/ GABA dysfunction. 🤯 SPS is assoc’d w/ both GABA antibodies & calcium dysfunction. We don’t yet know which comes 1st acquired Channelopathy or if it’s 2nd to GABA injury—either way Benzos have strong affinity for both GABA & Ca Ion Channels. @GeminiApp details “highly plausible— supported by current neuroimmunology— both acquired channelopathies & GABAergic pathways are deeply assoc’d w/ Stiff Person Syndrome (SPS). While classic SPS defined by an autoimmune attack on GABA pathway, downstream effects naturally create an "acquired channelopathy" state, & both mechanisms feed each other driving muscle stiffness acuity & spasms characteristic of SPS. [1, 2, 3, 4, 5] Scientific rationale for mechanistic link to SP detailed below. 1. GABA Neuro "Injury" is Direct Driver of SPS; functional "injury" to GABAergic system= metabolic shutdown caused by immune system. [6, 7, 8] •Synthesis Blockade: hallmark of classic SPS: high-titer anti-GAD65 antibodies. Glutamic Acid Decarboxylase (GAD), a rate-limiting enzyme req’d to convert glutamate into GABA. By blocking this enzyme, immune system starves CNS of its primary inhibitory neurotransmitter. [6, 9, 10, 11, 12] •Receptor & Structural Interruption: Other SPS antibody variants target GABA-A Receptor-Assoc Protein (GABARAP) or glycine receptors, directly breaking the machinery that allows neurons to receive inhibitory "relax" signals. [3, 13, 14] •Resulting Hyperexcitability: Without GABA acting as central nervous system's "brakes," alpha motor neurons in spinal cord fire continuously & uncontrollably. Lack of inhibition forces opposing muscle groups (agonists & antagonists) to contract simultaneously, generating rigid, board-like stiffness of SPS. [4, 6, 9, 15, 16] 2. Shift to an "Acquired" Ca Channelopathy, which occurs if an outside force—autoimmune response, toxicity, or chronic metabolic stress—alters how ion channels work. Connecting SPS in 2 major ways: [17, 18] •Downstream Ion Channel Dysregulation. [19, 20] •Autoantibody Overlap: combining a primary GABA deficit w/ an acquired channelopathy. [6, 13, 21, 22] Diagnostic & Therapeutic dual-pathway relationship explains why treating SPS reqs addressing 2 mechanisms simultaneously: 1Targeting the GABA Deficit: [13, 23] or 2Targeting the Channel Hyperactivity [24, 25] Heart-rate fluxes, dysautonomia etc [26] [1] [2] [3] [4] [5] [6] [7] [8] [9] [10] [11] [12] [13] [14] [15] [16] [17] [18] [19] [20] [21] [22] [23] [24] [25] [26] @_innercompass